Functions and Implications of Autophagy in Colon Cancer
Identifieur interne : 000928 ( Pmc/Corpus ); précédent : 000927; suivant : 000929Functions and Implications of Autophagy in Colon Cancer
Auteurs : Samantha N. Devenport ; Yatrik M. ShahSource :
- Cells [ 2073-4409 ] ; 2019.
Abstract
Autophagy is an essential function to breakdown cellular proteins and organelles to recycle for new nutrient building blocks. In colorectal cancer, the importance of autophagy is becoming widely recognized as it demonstrates both pro- and anti-tumorigenic functions. In colon cancer, cell autonomous and non-autonomous roles for autophagy are essential in growth and progression. However, the mechanisms downstream of autophagy (to reduce or enhance tumor growth) are not well known. Additionally, the signals that activate and coordinate autophagy for tumor cell growth and survival are not clear. Here, we highlight the context- and cargo-dependent role of autophagy in proliferation, cell death, and cargo breakdown.
Url:
DOI: 10.3390/cells8111349
PubMed: 31671556
PubMed Central: 6912527
Links to Exploration step
PMC:6912527Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Functions and Implications of Autophagy in Colon Cancer</title><author><name sortKey="Devenport, Samantha N" sort="Devenport, Samantha N" uniqKey="Devenport S" first="Samantha N" last="Devenport">Samantha N. Devenport</name><affiliation><nlm:aff id="af1-cells-08-01349">Cellular and Molecular Biology, University of Michigan, Ann Arbor, MI 48109, USA</nlm:aff></affiliation><affiliation><nlm:aff id="af2-cells-08-01349">Molecular and Integrative Physiology, Internal Medicine, Division of Gastroenterology, and Rogel Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA</nlm:aff></affiliation></author><author><name sortKey="Shah, Yatrik M" sort="Shah, Yatrik M" uniqKey="Shah Y" first="Yatrik M" last="Shah">Yatrik M. Shah</name><affiliation><nlm:aff id="af1-cells-08-01349">Cellular and Molecular Biology, University of Michigan, Ann Arbor, MI 48109, USA</nlm:aff></affiliation><affiliation><nlm:aff id="af2-cells-08-01349">Molecular and Integrative Physiology, Internal Medicine, Division of Gastroenterology, and Rogel Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31671556</idno><idno type="pmc">6912527</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6912527</idno><idno type="RBID">PMC:6912527</idno><idno type="doi">10.3390/cells8111349</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000928</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000928</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Functions and Implications of Autophagy in Colon Cancer</title><author><name sortKey="Devenport, Samantha N" sort="Devenport, Samantha N" uniqKey="Devenport S" first="Samantha N" last="Devenport">Samantha N. Devenport</name><affiliation><nlm:aff id="af1-cells-08-01349">Cellular and Molecular Biology, University of Michigan, Ann Arbor, MI 48109, USA</nlm:aff></affiliation><affiliation><nlm:aff id="af2-cells-08-01349">Molecular and Integrative Physiology, Internal Medicine, Division of Gastroenterology, and Rogel Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA</nlm:aff></affiliation></author><author><name sortKey="Shah, Yatrik M" sort="Shah, Yatrik M" uniqKey="Shah Y" first="Yatrik M" last="Shah">Yatrik M. Shah</name><affiliation><nlm:aff id="af1-cells-08-01349">Cellular and Molecular Biology, University of Michigan, Ann Arbor, MI 48109, USA</nlm:aff></affiliation><affiliation><nlm:aff id="af2-cells-08-01349">Molecular and Integrative Physiology, Internal Medicine, Division of Gastroenterology, and Rogel Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Cells</title><idno type="eISSN">2073-4409</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Autophagy is an essential function to breakdown cellular proteins and organelles to recycle for new nutrient building blocks. In colorectal cancer, the importance of autophagy is becoming widely recognized as it demonstrates both pro- and anti-tumorigenic functions. In colon cancer, cell autonomous and non-autonomous roles for autophagy are essential in growth and progression. However, the mechanisms downstream of autophagy (to reduce or enhance tumor growth) are not well known. Additionally, the signals that activate and coordinate autophagy for tumor cell growth and survival are not clear. Here, we highlight the context- and cargo-dependent role of autophagy in proliferation, cell death, and cargo breakdown.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Siegel, R L" uniqKey="Siegel R">R.L. Siegel</name></author><author><name sortKey="Miller, K D" uniqKey="Miller K">K.D. Miller</name></author><author><name sortKey="Fedewa, S A" uniqKey="Fedewa S">S.A. Fedewa</name></author><author><name sortKey="Ahnen, D J" uniqKey="Ahnen D">D.J. Ahnen</name></author><author><name sortKey="Meester, R G" uniqKey="Meester R">R.G. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Cells</journal-id><journal-id journal-id-type="iso-abbrev">Cells</journal-id><journal-id journal-id-type="publisher-id">cells</journal-id><journal-title-group><journal-title>Cells</journal-title></journal-title-group><issn pub-type="epub">2073-4409</issn><publisher><publisher-name>MDPI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31671556</article-id><article-id pub-id-type="pmc">6912527</article-id><article-id pub-id-type="doi">10.3390/cells8111349</article-id><article-id pub-id-type="publisher-id">cells-08-01349</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Functions and Implications of Autophagy in Colon Cancer</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Devenport</surname><given-names>Samantha N</given-names></name><xref ref-type="aff" rid="af1-cells-08-01349">1</xref><xref ref-type="aff" rid="af2-cells-08-01349">2</xref></contrib><contrib contrib-type="author"><name><surname>Shah</surname><given-names>Yatrik M</given-names></name><xref ref-type="aff" rid="af1-cells-08-01349">1</xref><xref ref-type="aff" rid="af2-cells-08-01349">2</xref><xref rid="c1-cells-08-01349" ref-type="corresp">*</xref></contrib></contrib-group><aff id="af1-cells-08-01349"><label>1</label>Cellular and Molecular Biology, University of Michigan, Ann Arbor, MI 48109, USA</aff><aff id="af2-cells-08-01349"><label>2</label>Molecular and Integrative Physiology, Internal Medicine, Division of Gastroenterology, and Rogel Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA</aff><author-notes><corresp id="c1-cells-08-01349"><label>*</label>Correspondence: <email>shahy@umich.edu</email>; Tel.: +1-734-615-0567</corresp></author-notes><pub-date pub-type="epub"><day>30</day><month>10</month><year>2019</year></pub-date><pub-date pub-type="collection"><month>11</month><year>2019</year></pub-date><volume>8</volume><issue>11</issue><elocation-id>1349</elocation-id><history><date date-type="received"><day>27</day><month>9</month><year>2019</year></date><date date-type="accepted"><day>28</day><month>10</month><year>2019</year></date></history><permissions><copyright-statement>© 2019 by the authors.</copyright-statement><copyright-year>2019</copyright-year><license license-type="open-access"><license-p>Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>).</license-p></license></permissions><abstract><p>Autophagy is an essential function to breakdown cellular proteins and organelles to recycle for new nutrient building blocks. In colorectal cancer, the importance of autophagy is becoming widely recognized as it demonstrates both pro- and anti-tumorigenic functions. In colon cancer, cell autonomous and non-autonomous roles for autophagy are essential in growth and progression. However, the mechanisms downstream of autophagy (to reduce or enhance tumor growth) are not well known. Additionally, the signals that activate and coordinate autophagy for tumor cell growth and survival are not clear. Here, we highlight the context- and cargo-dependent role of autophagy in proliferation, cell death, and cargo breakdown.</p></abstract><kwd-group><kwd>autophagy</kwd><kwd>nutrient</kwd><kwd>cancer</kwd><kwd>colon</kwd></kwd-group></article-meta></front><body><sec sec-type="intro" id="sec1-cells-08-01349"><title>1. Introduction</title><p>Colorectal cancer (CRC) is the third leading cause of cancer-related deaths in the United States. It is estimated that in 2018, over 140,000 people were diagnosed with CRC [<xref rid="B1-cells-08-01349" ref-type="bibr">1</xref>]. Survival rates have improved in the last three decades due to early detection, however patients diagnosed at later stages of disease have a 5-year survival rate of 14% [<xref rid="B2-cells-08-01349" ref-type="bibr">2</xref>,<xref rid="B3-cells-08-01349" ref-type="bibr">3</xref>]. Treatments available for these patients are limited, therefore it is important to better understand tumor development and identify targeted therapies to improve overall patient care. Sporadic CRCs are typically marked by the initial loss of the adenomatous polyposis coli (<italic>APC</italic>) gene. APC is a scaffold protein that leads to proteasomal degradation of β-catenin. Under active cell states, WNT ligands bind to its receptor frizzled and prevent β-catenin degradation and activate target genes. Loss of APC constitutively activates β-catenin and causes uncontrolled epithelial proliferation. Mutations in <italic>APC</italic> are typically followed by sequential mutations in tumor protein <italic>p53</italic> (p53), and mutations in <italic>KRAS</italic> leading to spontaneous tumor development and progression [<xref rid="B4-cells-08-01349" ref-type="bibr">4</xref>]. It is well known that chronic inflammatory diseases such as Crohn’s Disease or ulcerative colitis increase risk of developing colon cancer, referred to as colitis-associated cancer (CAC) [<xref rid="B5-cells-08-01349" ref-type="bibr">5</xref>,<xref rid="B6-cells-08-01349" ref-type="bibr">6</xref>]. CACs developed from inflammatory bowel diseases (IBD) are a rare subset. Moreover, <italic>p53</italic> mutations occur earlier in the progression of CAC and <italic>APC</italic> mutations are less frequent and are found in late stage tumors in comparison to sporadic CRC [<xref rid="B7-cells-08-01349" ref-type="bibr">7</xref>]. However, CAC provides a clear link between inflammation and tumor initiation.</p><p>Autophagy is a highly regulated process that degrades and recycles cellular components. Dysregulation of autophagy is implicated in many diseases (as reviewed in [<xref rid="B8-cells-08-01349" ref-type="bibr">8</xref>]). Under several different cell stressors, autophagy is activated through kinase signaling and transcriptional activation by serine/threonine protein kinase 1 (ULK1) and transcription factor EB (TFEB). This activates a cascade of autophagy-related genes (ATG) [<xref rid="B9-cells-08-01349" ref-type="bibr">9</xref>], and formation of a spherical double layer membrane termed the autophagosome. The autophagosome delivers key cytoplasmic cargo such as organelles, foreign bodies, and cellular components to the lysosome for degradation into macromolecules that can be utilized by the cell. In CRC, autophagy is known to play tumor promoting and tumor suppressive roles [<xref rid="B10-cells-08-01349" ref-type="bibr">10</xref>,<xref rid="B11-cells-08-01349" ref-type="bibr">11</xref>], but the underlying mechanisms are not well understood. Studies have found conflicting functions of autophagy in tumors. These discrepancies are typically due to differences in the cells and tumor models that are utilized [<xref rid="B12-cells-08-01349" ref-type="bibr">12</xref>,<xref rid="B13-cells-08-01349" ref-type="bibr">13</xref>,<xref rid="B14-cells-08-01349" ref-type="bibr">14</xref>,<xref rid="B15-cells-08-01349" ref-type="bibr">15</xref>]. Further study of autophagy and its prevalence in CRC will uncover its potential therapeutic use [<xref rid="B16-cells-08-01349" ref-type="bibr">16</xref>]. Here we highlight cellular pathways that regulate autophagy, selective forms of autophagy, and how these mechanisms target different cargo for degradation.</p></sec><sec id="sec2-cells-08-01349"><title>2. Autophagy Subtypes</title><p>Autophagy can be classified into three major subtypes; macro-autophagy, micro-autophagy, and chaperone-mediated autophagy. There is a need for better understanding of cellular cues and the cell-dependent context by which autophagic subtypes are co-opted in cancer cells for growth and survival.</p><sec id="sec2dot1-cells-08-01349"><title>2.1. Chaperone-Mediated Autophagy</title><p>Chaperone-mediated autophagy (CMA) differs from macro-autophagy in that select proteins are targeted for degradation by direct targeting to the lysosome. Proteins are recognized by heat shock cognate protein 70 (HSC70). HSC70 interacts with lysosome-associated membrane protein type 2A (LAMP-2A) to internalize proteins into the lysosome. CMA substrates contain a specific motif, KFERQ, which is essential for HSC70 binding [<xref rid="B17-cells-08-01349" ref-type="bibr">17</xref>]. Relevant to cancer, inhibition of macro-autophagy enhances CMA-dependent degradation of mutant p53 [<xref rid="B18-cells-08-01349" ref-type="bibr">18</xref>]. Increased expression of LAMP-2A demonstrated activated CMA in CRC [<xref rid="B19-cells-08-01349" ref-type="bibr">19</xref>]. These functions highlight a potential role of CMA in tumor development. However, these processes have not been well studied in CRC.</p></sec><sec id="sec2dot2-cells-08-01349"><title>2.2. Micro-Autophagy</title><p>Micro-autophagy is the direct engulfment of cellular components by invagination of the late endosome (<xref ref-type="fig" rid="cells-08-01349-f001">Figure 1</xref>). Broadly, the implications of micro-autophagy have not been studied in many cancer types. There is evidence in lung cancer that amino acid starvation, an important factor in cancer growth (discussed below), induces micro-autophagy [<xref rid="B20-cells-08-01349" ref-type="bibr">20</xref>]. However, the role of micro-autophagy in CRC has not been investigated in detail.</p></sec><sec id="sec2dot3-cells-08-01349"><title>2.3. Macro-Autophagy</title><p>Macro-autophagy can be broken down in to two subcategories that target cellular components for degradation; non-selective and selective. Non-selective macro-autophagy engulfs bulk cytosolic components and selective autophagy targets specific cargo for degradation (e.g., organelles and protein aggregates). For macro-autophagy, the phagophore, a precursor to the autophagosome, forms. Several ATG protein complexes are involved in early and late autophagosome formation [<xref rid="B21-cells-08-01349" ref-type="bibr">21</xref>]. As the membrane is forming, microtubule associated protein 1 light chain 3 beta (LC3-I) is conjugated with phosphatidylethanolamine and is processed into LC3-II [<xref rid="B22-cells-08-01349" ref-type="bibr">22</xref>]. Following fusion of the autophagosome with the lysosome, which contains the required enzymes for cargo degradation, LC3-II is broken down by the lysosome [<xref rid="B23-cells-08-01349" ref-type="bibr">23</xref>]. The turnover of LC3-II is often used as a readout of autophagic activity [<xref rid="B24-cells-08-01349" ref-type="bibr">24</xref>]. Here, we have provided a highly simplified overview of the complex process of macro-autophagy. This extremely coordinated event of cytoplasmic engulfment is generally activated in states of cell stress such as starvation. Anding and Baehrecke reviewed the important role of selective-autophagic processes in maintaining cellular homeostasis in response to stress [<xref rid="B25-cells-08-01349" ref-type="bibr">25</xref>]. Below we highlight the known selective-autophagic pathways and their potential role in CRC (<xref ref-type="fig" rid="cells-08-01349-f001">Figure 1</xref>).</p></sec><sec id="sec2dot4-cells-08-01349"><title>2.4. Mitophagy</title><p>Mitophagy is a process that selectively degrades mitochondria [<xref rid="B26-cells-08-01349" ref-type="bibr">26</xref>,<xref rid="B27-cells-08-01349" ref-type="bibr">27</xref>,<xref rid="B28-cells-08-01349" ref-type="bibr">28</xref>,<xref rid="B29-cells-08-01349" ref-type="bibr">29</xref>]. Mitophagy is highly evolutionarily conserved [<xref rid="B30-cells-08-01349" ref-type="bibr">30</xref>] and is known to be activated in yeast under starvation [<xref rid="B31-cells-08-01349" ref-type="bibr">31</xref>]. Therefore, highly proliferative cells under nutrient stress and starvation, such as cancer cells, may activate mitophagy. This process can be modulated by different pathways as discussed below.</p><sec id="sec2dot4dot1-cells-08-01349"><title>2.4.1. Parkin-Mediated Mitophagy</title><p>Under normal cell homeostasis, PTEN induced kinase 1 (PINK1) is maintained on the inner mitochondrial membrane. Upon damage or stress, PINK1 moves to the outer membrane and phosphorylates parkin (PRKN). This phosphorylation allows for ubiquitination of PRKN1 and targeting to the autophagosome. Poly-ubiquitination is recognized by adapters that direct mitochondria to the autophagosome. Known adapters include sequestosome (SQSTM1), neighbor of BRCA1 (NBR1), optineurin, nuclear domain 10 protein 52, and TAX1 binding protein; although, NBR1 is found to be non-essential for PRKN-mediated mitophagy [<xref rid="B26-cells-08-01349" ref-type="bibr">26</xref>,<xref rid="B32-cells-08-01349" ref-type="bibr">32</xref>,<xref rid="B33-cells-08-01349" ref-type="bibr">33</xref>]. Through this mechanism, a recent study found that in intestinal cancers, activation of mitophagy increased CD8+ T cells [<xref rid="B34-cells-08-01349" ref-type="bibr">34</xref>]. The upregulation of mitophagy causes an accumulation of iron followed by permeabilization of the lysosome. This permeabilization causes the release of proteases into the cytosol that induces presentation of MHC class I on the cell surface. This presentation elicits and an anti-tumor immune response by induction of CD8+ T-cells. In colitis, pharmacological induction of mitophagy through PRKN is found to inactivate inflammasomes in macrophages and ameliorate the impact of colitis [<xref rid="B35-cells-08-01349" ref-type="bibr">35</xref>,<xref rid="B36-cells-08-01349" ref-type="bibr">36</xref>,<xref rid="B37-cells-08-01349" ref-type="bibr">37</xref>]. While there are implications for PRKN-mediated mitophagy in CRC, one study found around 33% of colon tumors harbor PARK2 (the gene that encodes for PRKN) DNA copy number loss [<xref rid="B38-cells-08-01349" ref-type="bibr">38</xref>]. Interestingly, some colorectal cancer cell lines contain mutated forms of PRKN and may use alternate mechanisms to activate mitophagy [<xref rid="B38-cells-08-01349" ref-type="bibr">38</xref>]. Research is starting to investigate how PRKN may be used as a prognostic marker in CRC as it may correlate with invasion and overall survival [<xref rid="B39-cells-08-01349" ref-type="bibr">39</xref>].</p></sec><sec id="sec2dot4dot2-cells-08-01349"><title>2.4.2. Parkin-Independent Mitophagy</title><p>Alternatively to PRKN directed mitophagy, interaction of LC3 to FUN14 domain containing 1 (FUNDC1) protein located on the outer mitochondrial membrane can also initiate mitophagy [<xref rid="B40-cells-08-01349" ref-type="bibr">40</xref>]. Another PRKN-independent mechanism includes BCL2 interacting protein 3 (BNIP3), a critical receptor for mitophagy [<xref rid="B41-cells-08-01349" ref-type="bibr">41</xref>]. In breast cancer, BNIP3 loss promoted tumor progression and metastasis [<xref rid="B42-cells-08-01349" ref-type="bibr">42</xref>]. BNIP3 is induced by hypoxia signaling, a critical micro-environmental stressor in CRC (discussed below) [<xref rid="B43-cells-08-01349" ref-type="bibr">43</xref>]. The impact of BNIP3 and mitophagy in CRC have not been studied in detail. The known function in breast cancer, and BNIP3’s relationship with hypoxia signaling provides a foundation to investigate the role in CRC. Mitochondria may also be recruited to the autophagosome by FKBP8, a member of the FK506-binding protein family. FKBP8 is located on the outer membrane and has an anti-apoptotic role by interacting with Bcl-2 [<xref rid="B44-cells-08-01349" ref-type="bibr">44</xref>]. PRKN-independent mitophagy can be initiated by binding of LC3A to FKBP8 [<xref rid="B45-cells-08-01349" ref-type="bibr">45</xref>]. Additional mechanisms of PRKN-independent mitochondrial control are reviewed by Stockum et al. [<xref rid="B46-cells-08-01349" ref-type="bibr">46</xref>]. PRKN-independent mechanisms, and the evidence of mutated PRKN discussed above in CRC highlight the potential importance of investigating PRKN- independent mitophagy in CRC.</p><p>Pharmacological targeting of mitochondria with Mito-CP or Mito-Met<sub>10</sub> in <italic>KRAS</italic> mutant colorectal cancers induced mitophagy and decreased cell proliferation [<xref rid="B47-cells-08-01349" ref-type="bibr">47</xref>]. In colon cancer, treatment with a BH3 mimetic, which inhibits Bcl-2 anti-apoptotic proteins, induced mitophagy. Treatment with the mimetic, in combination with an mitophagy inhibitor, reduced CRC cell growth [<xref rid="B48-cells-08-01349" ref-type="bibr">48</xref>]. However, conflicting roles of mitophagy have been noted in cancer (Reviewed in [<xref rid="B49-cells-08-01349" ref-type="bibr">49</xref>]). Treatment with the mitophagy inhibitor liensinine increased breast cancer cell death [<xref rid="B50-cells-08-01349" ref-type="bibr">50</xref>]. Conversely, activation of mitophagy with ceramide, a molecule involved in sphingolipid metabolism, reduced tumor burden in acute myeloid leukemia [<xref rid="B51-cells-08-01349" ref-type="bibr">51</xref>]. In-depth understanding of mitophagy in CRC is needed in order to develop better therapies that can target mitophagy to reduce tumor growth.</p></sec></sec><sec id="sec2dot5-cells-08-01349"><title>2.5. Ribophagy</title><p>Ribophagy is the breakdown of ribosomes in cells, which constitute 10% of total cellular protein. Ribophagy is extremely low basally in cells [<xref rid="B52-cells-08-01349" ref-type="bibr">52</xref>]. Initiation of ribophagy occurs by the binding of nuclear FMR1 interacting protein 1 (NUFIP1) to ribosomes. This interaction leads to autophagosome recruitment by LC3 [<xref rid="B53-cells-08-01349" ref-type="bibr">53</xref>]. Starvation or molecular target of rapamycin complex 1 (mTORC1) inhibition induced NUFIP1 activity and increased ribophagy [<xref rid="B53-cells-08-01349" ref-type="bibr">53</xref>]. Breakdown of ribosomes under starvation underscores the importance of ribophagy for cellular nutrient maintenance. However, non-selective bulk degradation of ribosomes may also be utilized [<xref rid="B52-cells-08-01349" ref-type="bibr">52</xref>]. Little information is known about ribophagy in cancer. However, ribosomes contain a large amount of amino acids and nucleotides and can potentially serve as a nutrient store in the tumor environment.</p></sec><sec id="sec2dot6-cells-08-01349"><title>2.6. Proteophagy</title><p>Clearance of proteasomes through autophagy is known as proteophagy. Cross-talk between the proteasome and autophagy is found under nitrogen starvation in cells wherein autophagy degrades ribosomes (and proteasomes) under nutrient starvation [<xref rid="B54-cells-08-01349" ref-type="bibr">54</xref>]. One of the earliest citations of proteophagy suggests that this process occurs through a chaperone-mediated mechanism where the proteasome is targeted to the lysosome by HSC73 [<xref rid="B55-cells-08-01349" ref-type="bibr">55</xref>]. More recent work uncovers the sequestration of the proteasome in autophagosomes under cell stress, suggesting proteophagy can occur in a macro-autophagy or CMA driven fashion [<xref rid="B56-cells-08-01349" ref-type="bibr">56</xref>]. Currently there is no data to suggest that proteophagy is activated in cancer.</p></sec><sec id="sec2dot7-cells-08-01349"><title>2.7. Pexophagy</title><p>Peroxisomes are small organelle structures that break down fatty acids in the cytoplasm. The degradation of these products through autophagy requires SQSTM1 and NBR1 [<xref rid="B57-cells-08-01349" ref-type="bibr">57</xref>]. In healthy liver, loss of autophagy through ATG7 led to a buildup of peroxisomes [<xref rid="B58-cells-08-01349" ref-type="bibr">58</xref>]. Under starvation conditions, ubiquitination of peroxisomes occurred by peroxisomal biogenesis factor 2 (PEX2) in HeLa cells and mouse embryonic fibroblasts [<xref rid="B59-cells-08-01349" ref-type="bibr">59</xref>]. To our knowledge, the utilization of pexophagy in CRC has yet to be investigated. However, hypoxia inducible factor-2α (HIF-2α), an important transcription factor in CRC (discussed below), was found to promote pexophagy in hepatocytes [<xref rid="B60-cells-08-01349" ref-type="bibr">60</xref>]. While these findings were not investigated in colon tissue, the activation of pexophagy under starvation and hypoxia highlights the potential importance of studying pexophagy in CRC.</p></sec><sec id="sec2dot8-cells-08-01349"><title>2.8. Ferritinophagy</title><p>Iron storage protein ferritin is broken down by the lysosome for iron release and cellular iron utilization. This degradation is directed by the nuclear receptor coactivator 4 (NCOA4) [<xref rid="B61-cells-08-01349" ref-type="bibr">61</xref>]. Interestingly, ferritinophagy is required for induction of ferroptosis, a form of cell death that requires iron [<xref rid="B62-cells-08-01349" ref-type="bibr">62</xref>,<xref rid="B63-cells-08-01349" ref-type="bibr">63</xref>]. Certain cancers have shown a sensitivity to ferroptosis [<xref rid="B64-cells-08-01349" ref-type="bibr">64</xref>] and pharmacological induction of ferroptosis is found to reduce pancreatic and hepatic cancer cell growth [<xref rid="B63-cells-08-01349" ref-type="bibr">63</xref>,<xref rid="B65-cells-08-01349" ref-type="bibr">65</xref>]. While little work has been done to investigate the importance of ferritinophagy in CRC, the essential role of iron in CRC growth [<xref rid="B66-cells-08-01349" ref-type="bibr">66</xref>] and the sensitivity of different cancer types to ferroptosis [<xref rid="B67-cells-08-01349" ref-type="bibr">67</xref>] highlights the importance in studying ferritin turnover in CRC.</p></sec><sec id="sec2dot9-cells-08-01349"><title>2.9. Xenophagy</title><p>Xenophagy is a process initiated by the cell for protection against pathogens. Phagophores engulf pathogens and fuse to the autophagosome for breakdown by autophagy. Xenophagy can play a particularly important role in the colon due to the host-microbiome interaction. Protection from intestinal epithelial infection requires the autophagy gene <italic>ATG16L1</italic> [<xref rid="B68-cells-08-01349" ref-type="bibr">68</xref>]. Recent screening of xenophagy effectors identified a V-ATPase and ATG16L1 mechanism to specifically activate xenophagy under bacterial infiltration [<xref rid="B69-cells-08-01349" ref-type="bibr">69</xref>]. Certain bacteria can be targeted by SQSTM1, an important protein in autophagy [<xref rid="B70-cells-08-01349" ref-type="bibr">70</xref>]. In Crohn’s Disease, the stimulation of xenophagy using resveratrol reduced <italic>Salmonella Typhimurium</italic>, an enteric pathogen associated with Crohn’s Disease [<xref rid="B71-cells-08-01349" ref-type="bibr">71</xref>]. When colon cancer cells are treated with two mircoRNAs, MIR106B and MIR93, reduced ATG16L1 prevented removal of intracellular bacteria from epithelial cells via autophagy [<xref rid="B72-cells-08-01349" ref-type="bibr">72</xref>]. As mentioned, patients with Crohn’s Disease have an increased risk of developing CAC and this is partially due to bacterial infiltration. Understanding the role of xenophagy in host-microbiome homeostasis may be essential in characterizing the microbiota-tumor interaction.</p></sec></sec><sec id="sec3-cells-08-01349"><title>3. Role of Autophagy in CRC</title><p>It is important to understand the role of autophagy at different stages and under different mutational loads to properly target tumors. A clinical study observed down-regulation of <italic>ATG5</italic> in CRC patients. However, increased expression correlated with increased incidence of invasion [<xref rid="B73-cells-08-01349" ref-type="bibr">73</xref>]. Conversely, expression of LC3B and SQSTM1 correlated with poor prognosis [<xref rid="B74-cells-08-01349" ref-type="bibr">74</xref>]. In mouse models, loss of <italic>Atg7</italic> in intestinal epithelial cells inhibited tumor growth through an immune response elicited by the microbiome [<xref rid="B75-cells-08-01349" ref-type="bibr">75</xref>]. Additionally, receptor for activated C kinase 1 (RACK1), a commonly found mutation in cancer, induced autophagy and promoted proliferation while inhibiting apoptosis in colon cancer [<xref rid="B76-cells-08-01349" ref-type="bibr">76</xref>]. Autophagy also modulated the degradation of the transcription factor FOXO3a in CRC. Inhibition of autophagy elevated levels of FOXO3a and led to transcriptional upregulation of pro-apoptotic genes [<xref rid="B77-cells-08-01349" ref-type="bibr">77</xref>]. Apoptosis also increased when autophagy was inhibited in CRC cells following activation of p53 and endoplasmic reticulum stress [<xref rid="B78-cells-08-01349" ref-type="bibr">78</xref>]. Conversely, treatment with Brevlin A increased autophagy and decreased tumor size [<xref rid="B79-cells-08-01349" ref-type="bibr">79</xref>]. This brief overview emphasizes the complexity of autophagy in CRC. It remains unclear if autophagy is anti- or pro- tumorigenic and in-depth mechanistic studies are needed. <xref rid="cells-08-01349-t001" ref-type="table">Table 1</xref> outlines some of the opposing roles of autophagy in CRC.</p><p>An understanding of mutations in autophagy-associated genes, how autophagy is altered by increased mutational load, or via specific tumor suppressors or oncogenes is essential in assessing its role in tumor development. In CRC, there is low frequency of mutations in autophagy-associated genes [<xref rid="B90-cells-08-01349" ref-type="bibr">90</xref>]. In a small cohort of patient samples, tumors expressed decreased levels of ATG5, however increased expression correlated with invasion into lymphovascular tissue [<xref rid="B73-cells-08-01349" ref-type="bibr">73</xref>]. A study demonstrated that 95% of colon tumors expressed higher Beclin-1 compared to normal tissue [<xref rid="B80-cells-08-01349" ref-type="bibr">80</xref>]. These studies suggest that autophagy is important in cancer development. Similarly, in mutant <italic>KRAS</italic> cancers, autophagy induction occurred under starvation. Inhibition of <italic>KRAS</italic> reduced autophagy in these cells and inhibited cell growth [<xref rid="B84-cells-08-01349" ref-type="bibr">84</xref>]. In CRC-derived cell lines, p53 promoted the degradation of LC3 allowing for stable autophagic flux [<xref rid="B81-cells-08-01349" ref-type="bibr">81</xref>]. With loss of p53, LC3 accumulated and led to apoptosis. In CRCs with high microsatellite instability, 27% of the cancers harbored at least one mutation in either <italic>ATG2B</italic>, <italic>ATG5</italic>, <italic>ATG9B</italic>, or <italic>ATG12</italic> [<xref rid="B91-cells-08-01349" ref-type="bibr">91</xref>]. Additionally, a study aimed to understand responsiveness to therapy in BRAF (a protein involved in RAS/MAPK signaling) mutant colon cancers found that treatment with EGFR antibodies and checkpoint inhibitors induced autophagy and combining these treatments with an autophagy inhibitor reduced CRC cell growth [<xref rid="B92-cells-08-01349" ref-type="bibr">92</xref>]. Patients with Crohn’s Disease have an increased chance of developing CAC. Deficiencies in the response to bacterial sensing and invasion were observed following loss of autophagy through impairment in nucleotide-binding oligomerization domain (NOD1/2) signaling [<xref rid="B93-cells-08-01349" ref-type="bibr">93</xref>]. Loss of autophagy or mutations in autophagic genes may increase bacterial infiltration, which can impact the development of CAC. Mutations in autophagy-associated genes, or regulation of autophagy through mutations in genes such as <italic>KRAS</italic> and <italic>p53</italic>, demonstrate the important role of this mechanism in CRC. To begin addressing how autophagy can be used clinically, researchers have found a gene signature based on nine autophagy related genes that can accurately predict survival in colon cancer [<xref rid="B94-cells-08-01349" ref-type="bibr">94</xref>].</p><p>Histone deacetylase inhibitors as stand-alone or adjuvant therapies are currently used in several cancers [<xref rid="B95-cells-08-01349" ref-type="bibr">95</xref>]. In colorectal cancer cells, inhibition of autophagy through chloroquine, in combination with the histone deacetylase inhibitor vorinostat, led to an accumulation of ubiquitinated proteins and increased cell death [<xref rid="B85-cells-08-01349" ref-type="bibr">85</xref>]. Additionally, chemo-resistance required decreased autophagy in 5-fluorouracil (a common chemotherapeutic for CRC) resistant cells [<xref rid="B86-cells-08-01349" ref-type="bibr">86</xref>]. The authors speculated, that this observation was due to low autophagy resulting in accumulation of tumor promoting oxidative stress, inflammation, and damaged mitochondria.</p><p>CRC consist of multiple epithelial cell types as well as infiltrating immune cells. In IBD it is clear that dysregulation of autophagy in Paneth cells impacts tissue injury and inflammation [<xref rid="B96-cells-08-01349" ref-type="bibr">96</xref>]. However, cell type specificity of autophagy in tumor growth is unclear.</p><p>Immune cell autophagy: The anti-tumor immune response can directly kill cancer cells. As the tumor progresses, the microenvironment shifts to a highly immunosuppressive state and many of the immune cells potentiate tumor growth. Immunosuppression is essential in enhancing tumor progression, and immune cells can employ autophagy to perform standard functions including antigen presentation and cytokine production (Reviewed in [<xref rid="B97-cells-08-01349" ref-type="bibr">97</xref>]). In tumor-associated macrophages (TAM)s, upregulation of autophagy reduced tumor growth and increased apoptosis in CRC cells. Moreover, radiosensitization of CRC required increased autophagy in TAMs [<xref rid="B98-cells-08-01349" ref-type="bibr">98</xref>]. Conversely, when autophagy is lost in regulatory T-cells by disrupting <italic>Atg7</italic>, there was impaired ability of the anti-tumor immune response to CRC cells [<xref rid="B99-cells-08-01349" ref-type="bibr">99</xref>]. This was due in part by increased apoptosis in the T-cells. While not specifically studied in colon cancer, different immune cells including neutrophils, macrophages, B-cells, and natural killer cells rely on autophagy for their development and function (Reviewed in [<xref rid="B100-cells-08-01349" ref-type="bibr">100</xref>]). Immune cell specific autophagy underscore the importance of investigating this pathway in different cell types to better develop strategies for modulating tumor growth. </p><p>Epithelial autophagy: Tumor epithelial autophagy in <italic>KRAS</italic>-driven cancers alters inflammatory mediators to suppress the immune response [<xref rid="B82-cells-08-01349" ref-type="bibr">82</xref>]. Furthermore, inhibition of autophagy in cancer cells blocked interferon gamma-mediated cell death [<xref rid="B101-cells-08-01349" ref-type="bibr">101</xref>]. The role of the immune system and its interaction with the gut microbiota is important in tumor development. Cell autonomous autophagy in healthy epithelial cells altered barrier function by breaking down junctional proteins such as claudin 2 [<xref rid="B102-cells-08-01349" ref-type="bibr">102</xref>]. Impaired barrier function can lead to increased bacterial infiltration to cause inflammation and damage in the gut. Recent work demonstrated tumor stage specific changes in bacterial infiltration, inflammatory signaling and cancer progression and growth in CRC [<xref rid="B103-cells-08-01349" ref-type="bibr">103</xref>]. This suggests a possible role of epithelial xenophagy in CRC. In CRC tumors, regulatory T-cell infiltration inversely correlated with SQSTM1 expression [<xref rid="B104-cells-08-01349" ref-type="bibr">104</xref>]. The utilization of autophagy in epithelial cells may alter recruitment or function of the immune response. In summary there are major differences in the direct impact of autophagy in epithelial cells, immune cells, or the heterocellular cross-talk between these cells that can impact CRC growth and progression (<xref ref-type="fig" rid="cells-08-01349-f002">Figure 2</xref>). Understanding the changes in autophagy and how it impacts tumor response will allow researchers to further understand these mechanisms in different cell types.</p></sec><sec id="sec4-cells-08-01349"><title>4. Cellular Cues for Autophagic Activation in Cancer</title><sec id="sec4dot1-cells-08-01349"><title>4.1. Starvation</title><p>The highly proliferative nature of tumors leads to a reduction in availability of nutrients in the microenvironment. In cancer, hyper-activation of mTORC1, a known pathway of nutrient sensing, contributes to cell proliferation and tumor progression. mTORC1 is activated in about 50% of CRC tumors. <xref ref-type="fig" rid="cells-08-01349-f003">Figure 3</xref>A outlines the known mechanistic cross-talk in CRC between autophagy and mTORC1. In conditions where amino acids are abundant, mTORC1 is localized to the lysosomal membrane (Reviewed in [<xref rid="B105-cells-08-01349" ref-type="bibr">105</xref>]). Hypoxic induction of DNA damage inducible transcript 4 (REDD1) signaling has been shown to regulate mTORC1 through truncation of the hemartin (Tsc1/Tsc2) complex [<xref rid="B106-cells-08-01349" ref-type="bibr">106</xref>]. Since mTORC1 is activated by available nutrients, a feedback loop exists between these two mechanisms wherein autophagy generates new macromolecules to activate mTORC1. The cross-talk between these two mechanisms are essential in maintaining cell growth and proliferation [<xref rid="B106-cells-08-01349" ref-type="bibr">106</xref>]. Importantly, mTORC1 is integrated to the autophagic pathway via activation of TFEB and ULK1-ATG13-FIP200 (Family kinase-interacting protein of 200 kDa) complex [<xref rid="B107-cells-08-01349" ref-type="bibr">107</xref>,<xref rid="B108-cells-08-01349" ref-type="bibr">108</xref>]. Independent of mTORC1, AMPK activated the ULK1 complex under starvation [<xref rid="B109-cells-08-01349" ref-type="bibr">109</xref>]. Under nutrient rich conditions mTORC1 phosphorylated ULK1 and inhibited the ULK1-AMPK interaction to block autophagy [<xref rid="B109-cells-08-01349" ref-type="bibr">109</xref>]. It is important to consider that the TFEB, ULK1, and AMPK pathways are known to be regulated by amino acids, which contributes to another mode of autophagy regulation [<xref rid="B110-cells-08-01349" ref-type="bibr">110</xref>]. In a model of lung cancer, amino acid starvation led to an induction of non-selective macro-autophagy. However, amino acid starvation has been shown independent of mTORC1 to induce micro-autophagy that directly engulfs receptors of selective autophagy including NCOA4, LC3B, and SQSTM1 into endosomes [<xref rid="B20-cells-08-01349" ref-type="bibr">20</xref>]. The authors suggest these functions may prevent selective macro-autophagy and promote non-selective autophagy under starvation. Interestingly, under leucine starvation, a cleaved form of SQSTM1 is generated by the protease caspase-8. Under starvation when autophagy is active, a portion of the available SQSTM1 is cleaved. In nutrient replete conditions, this cleaved protein activates mTORC1 to increase leucine sensing [<xref rid="B111-cells-08-01349" ref-type="bibr">111</xref>]. The cleaved SQSTM1 is not able to participate in autophagy preventing opposing functions between mTORC1 and autophagy. Moreover, in ovarian cancer cells, arginine deprivation activated autophagy to promote cell survival [<xref rid="B112-cells-08-01349" ref-type="bibr">112</xref>]. Inhibition of autophagy both chemically or genetically significantly reduced cell growth. While these studies were not in CRC, these findings highlight the potential of combinatorial therapeutics with autophagy inhibitors and treatments such as arginase for tumors that rely on arginine for growth [<xref rid="B112-cells-08-01349" ref-type="bibr">112</xref>]. Glucose uptake plays a critical role in the growth of many cancer types, including CRC. In glucose-free conditions, knock-down of autophagy-associated genes increased cell death [<xref rid="B113-cells-08-01349" ref-type="bibr">113</xref>]. Similarly, when colon cancer spheroids were stressed under restricted glucose or serum an increase in autophagy was observed [<xref rid="B114-cells-08-01349" ref-type="bibr">114</xref>]. Under similar starvation conditions, <italic>Kras</italic> mutant tumors require autophagy for oxidative metabolism [<xref rid="B115-cells-08-01349" ref-type="bibr">115</xref>]. Starvation also affected expression of claudin 1 in colon cancer. Expression of claudin 1 was higher in tumor tissue and showed co-staining with lysosomal markers LAMP1 and 2 with increased autophagy. Under starvation, claudin 1 expression increased mediating a reduction in SQSTM1. This suppression suggests claudin 1 cross-talks with autophagy under starvation [<xref rid="B116-cells-08-01349" ref-type="bibr">116</xref>]. When and how nutrient availability impacts autophagy is essential in understanding its function in CRC tumors (<xref ref-type="fig" rid="cells-08-01349-f003">Figure 3</xref>B).</p></sec><sec id="sec4dot2-cells-08-01349"><title>4.2. Hypoxia</title><p>Hypoxia plays a key role in CRC development and progression. Hypoxia signaling is mediated by two transcription factors, hypoxia-inducible factor (HIF)-1α and HIF-2α, which have overlapping and distinct functions. In CRC, HIF-2α (not HIF-1α) is essential for CRC growth and progression [<xref rid="B117-cells-08-01349" ref-type="bibr">117</xref>]. Hypoxia is a well conserved cell stress that activates autophagy [<xref rid="B43-cells-08-01349" ref-type="bibr">43</xref>]. In tumor hypoxic foci, autophagy levels are highly elevated but rapidly subside upon establishment of a blood supply [<xref rid="B118-cells-08-01349" ref-type="bibr">118</xref>]. In colon cancer there is a known connection between hypoxia and mitophagy. Hypoxia disrupted mitochondrial respiration leading to increased mitophagy (<xref ref-type="fig" rid="cells-08-01349-f002">Figure 2</xref>) [<xref rid="B119-cells-08-01349" ref-type="bibr">119</xref>]. Moreover, HIF-1α upregulated BNIP3 to induce mitophagy [<xref rid="B43-cells-08-01349" ref-type="bibr">43</xref>]. In patient derived CRC cells, inhibition of autophagy with 3-Methyladenin in combination with hypoxia, increased apoptotic death in cancer cells [<xref rid="B120-cells-08-01349" ref-type="bibr">120</xref>]. Moreover, the micro RNA miR-20a was found to inhibit hypoxia induced autophagy [<xref rid="B121-cells-08-01349" ref-type="bibr">121</xref>]. Additionally, in glioblastoma, HIF-1α induced autophagy and drove tumor growth [<xref rid="B122-cells-08-01349" ref-type="bibr">122</xref>]. HIF-1α does not alter CRC tumorigenesis in mouse models [<xref rid="B117-cells-08-01349" ref-type="bibr">117</xref>], however it will be interesting to assess if HIF-2α has overlapping roles in the context of autophagy.</p></sec><sec id="sec4dot3-cells-08-01349"><title>4.3. Microbiota</title><p>As highlighted briefly above, autophagy can play an important role through xenophagy in managing the host–microbiome interaction. Moreover, dysregulation of autophagy is well characterized in IBD. New work studying chronic colitis suggests that autophagy protected cells by reducing apoptosis through upregulation of tumor necrosis factor-α [<xref rid="B123-cells-08-01349" ref-type="bibr">123</xref>]. As discussed above, the importance of autophagy specifically in Paneth cells is known [<xref rid="B96-cells-08-01349" ref-type="bibr">96</xref>]. In healthy tissue, induction of autophagy in Paneth cells induced interferon gamma to protect against microbiota. However, when this mechanism is lost, intestinal inflammation is exacerbated [<xref rid="B124-cells-08-01349" ref-type="bibr">124</xref>]. Consistent with data from IBD, the heterocellular cross-talk with microbiota is a major factor in tumor-elicited inflammation in CRC. When microbiome composition is altered under chronic inflammation or barrier defects, changes in the inflammatory response altered tumorigenesis [<xref rid="B125-cells-08-01349" ref-type="bibr">125</xref>,<xref rid="B126-cells-08-01349" ref-type="bibr">126</xref>]. The cross-talk between the microbiota and immune system highlights the complexity of the tumor microenvironment in the colon [<xref rid="B127-cells-08-01349" ref-type="bibr">127</xref>,<xref rid="B128-cells-08-01349" ref-type="bibr">128</xref>]. The importance of these mechanisms have been studied in depth [<xref rid="B129-cells-08-01349" ref-type="bibr">129</xref>,<xref rid="B130-cells-08-01349" ref-type="bibr">130</xref>]. Loss of autophagy in healthy colon epithelial cells through <italic>Atg5</italic> disruption altered the composition of the gut microbiota and the gut immune response suggesting implications in chronic colitis [<xref rid="B131-cells-08-01349" ref-type="bibr">131</xref>]. Similarly, loss of <italic>Atg7</italic> in intestinal epithelial cells and tumor tissue led to infiltration of anti-tumor immune cells decreasing tumor burden [<xref rid="B75-cells-08-01349" ref-type="bibr">75</xref>]. Treatment with antibiotics attenuated this response, further supporting a novel integration of microbiota and autophagy in tumor growth. It is important to highlight that this work utilized an <italic>Apc</italic> model where tumor suppressor p53 was intact. In many cancers, however, p53 is deleted or mutated thus these findings may only be applicable to patients with wild-type p53 [<xref rid="B75-cells-08-01349" ref-type="bibr">75</xref>]. In summary, the above findings highlight the cross-talk between the microbiota and autophagy. Further mechanistic studies may uncover novel therapeutic approaches targeting autophagy and microbiota.</p></sec></sec><sec id="sec5-cells-08-01349"><title>5. Autophagic Substrates</title><p>The broad use of autophagy to meet metabolic demands is reviewed by Rabinowitz and White [<xref rid="B132-cells-08-01349" ref-type="bibr">132</xref>]. Autophagy in normal cell physiology is critical to maintain amino acid levels [<xref rid="B133-cells-08-01349" ref-type="bibr">133</xref>]. While it is thought that the products of autophagic degradation are recycled for use in cancer, in CRC the substrates targeted for autophagy and how the degradative products are utilized is not clear. In cancer, autophagy can degrade macromolecules for nutrients, and degrade tumor suppressors or oncogenes to alter growth. Below we outline both of these functions.</p><p>Previous literature has found an increase in autophagy in CRC spheroids under glucose or serum restriction [<xref rid="B114-cells-08-01349" ref-type="bibr">114</xref>]. However, the degradative products of this process are unknown. A study investigated this question by studying loss of <italic>ATG5</italic> in <italic>RAS</italic>-driven cancer cells. Loss of <italic>ATG5</italic> showed global changes in the proteome. Inhibition of autophagy, in combination with starvation, increased endoplasmic reticulum chaperones, proteins involved in DNA replication, and Rig-I like receptor signaling pathway. However, proteins that are known to be essential in stress survival were not altered with autophagy inhibition under starvation conditions [<xref rid="B82-cells-08-01349" ref-type="bibr">82</xref>]. This work uncovers how autophagy impacts cellular response to stresses such as starvation that are observed in the tumor microenvironment. Additionally, in <italic>RAS</italic>-driven cancers, autophagy drove glycolysis [<xref rid="B83-cells-08-01349" ref-type="bibr">83</xref>]. Degradation of cellular components into amino acids is essential for cancer utilization. Thomas and colleagues demonstrated that amino acid levels in starved breast cancer cells increased with activated autophagy, whereas normal cells maintained amino acid levels under starvation. It is hypothesized that this is due to the high nutrient demand to maintain the proliferation rates of the cancer cells [<xref rid="B134-cells-08-01349" ref-type="bibr">134</xref>]. While this study was not in CRC this underscores the importance of understanding how autophagy is used for nutrient acquisition.</p><p>While autophagy may be employed to acquire nutrients, it has been shown to break down proteins that activate or block tumor growth. Autophagy can cause the degradation of dishevelled in colon cancer and contribute to the activation of Wnt signaling, thus promoting tumor growth [<xref rid="B135-cells-08-01349" ref-type="bibr">135</xref>]. Similarly in CRC, the cancerous inhibitor of protein phosphatase 2a (CIP2A) is overexpressed [<xref rid="B136-cells-08-01349" ref-type="bibr">136</xref>]. CIP2a is involved in Myc protein stability. Temsirolimus, an FDA approved mTORC1 inhibitor that activates autophagy led to degradation of CIP2a and cell death in CRC [<xref rid="B87-cells-08-01349" ref-type="bibr">87</xref>]. In colon cancer, CyclinD1 is highly expressed and contributes to hyper-proliferation. Estrogen receptor beta was shown to activate autophagy and cause the breakdown of CyclinD1 causing cell cycle arrest and tumor death [<xref rid="B88-cells-08-01349" ref-type="bibr">88</xref>]. To prevent growth, treatment with 4-hydroxytamoxifen caused degradation of KRAS through autophagy in colon cancer [<xref rid="B89-cells-08-01349" ref-type="bibr">89</xref>]. As mentioned previously, basal autophagy breaks down FOXO3a to prevent apoptosis in CRC, to promote tumor growth [<xref rid="B77-cells-08-01349" ref-type="bibr">77</xref>]. While some work has been done, the process of breaking down proteins to inhibit or promote tumor growth are not well studied. A thorough understanding of autophagy in the context of CRC is important in targeting these mechanisms.</p></sec><sec sec-type="conclusions" id="sec6-cells-08-01349"><title>6. Conclusions and Future Perspectives</title><p>In general, non-selective autophagy is used for nutrient stress while selective autophagy is used for cell maintenance. However, in the context of tumor growth in CRC or CAC, these roles may change. Understanding the autophagic substrates that are recycled and how those substrates are utilized in tumor growth and development will identify ideal targets for treatments. While we have discussed mechanisms by which tumor cells may obtain nutrients through autophagy, these mechanisms are not clearly defined in CRC. The cross-talk between hypoxia and mitophagy underscores the importance of these mechanisms in CRC. Identifying the role of selective autophagy for tumor growth will allow the development of targeted therapeutics for CRC. The potential importance of mitophagy in cell stress and nutrient availability highlights a potential target in cancers. Moreover, if tumor cells employ selective autophagy for growth and survival, these mechanisms may be targets for vulnerability in CRC. Some of these approaches are reviewed by Martins and Baptista [<xref rid="B137-cells-08-01349" ref-type="bibr">137</xref>]. Additionally, we have highlighted the cell type specific contributions of autophagy and more precise work on cell type specific dependency on autophagy will shed light on the mechanistic role of autophagy in tumor development. More directly, the pathways activated or inhibited during nutrient stress and how autophagic substrates are being utilized in cancer cells will be critical to understanding the pleiotropic role of autophagy in cancer growth and progression.</p></sec></body><back><notes><title>Author Contributions</title><p>All authors contributed to writing and editing this manuscript.</p></notes><notes><title>Funding</title><p>This work was supported by the NIH, R01CA148828 and R01DK095201 to Y.M.S, and T32GM007315 and T32CA140044 to S.N.D.</p></notes><notes notes-type="COI-statement"><title>Conflicts of Interest</title><p>The authors declare no conflict of interest.</p></notes><ref-list><title>References</title><ref id="B1-cells-08-01349"><label>1.</label><element-citation publication-type="book"><person-group person-group-type="author"><collab>National Cancer Institute</collab></person-group><source>Surveillance, Epidemiology, and End Results (SEER) Program Research Data (1973–2014)</source><publisher-name>S.R.P. 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Specifically, highlighting examples of selective macro-autophagy.</p></caption><graphic xlink:href="cells-08-01349-g001"></graphic></fig><fig id="cells-08-01349-f002" orientation="portrait" position="float"><label>Figure 2</label><caption><p>Schematic of the tumor microenvironment highlighting the impact of autophagy. Cell autonomous roles of autophagy in immune, epithelial or, the cross-talk between cell types in colorectal cancer.</p></caption><graphic xlink:href="cells-08-01349-g002"></graphic></fig><fig id="cells-08-01349-f003" orientation="portrait" position="float"><label>Figure 3</label><caption><p>Schematic summarizing (<bold>A</bold>) Simplified overview of mechanisms of mTORC1 regulation. and (<bold>B</bold>) how nutrient modulation impacts autophagy. Bolded mechanisms indicate data from non-CRC samples. Please refer to text for detailed mechanisms.</p></caption><graphic xlink:href="cells-08-01349-g003"></graphic></fig><table-wrap id="cells-08-01349-t001" orientation="portrait" position="float"><object-id pub-id-type="pii">cells-08-01349-t001_Table 1</object-id><label>Table 1</label><caption><p>Functions of autophagy in CRC. <bold>A</bold>. Observation/Autophagy indicates what mechanisms are observed in CRC tumors and if autophagy is active or inactive. Tumor response is a summary of whether or not the autophagy activity indicated generates a pro- or anti- tumor response. <bold>B</bold>. Summary of therapies and their modulation of autophagy. Treatment: Which therapy was employed. Autophagy: how the stated therapy modulated autophagy activation. Tumor response: how manipulation of autophagy via therapeutic treatment impacted tumor growth.</p></caption><table frame="hsides" rules="groups"><tbody><tr><td colspan="5" align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1"><bold>A</bold></td></tr><tr><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>Observation</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>Autophagy</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>Tumor response</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>Reference</bold></td></tr><tr><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>Activated chaperone-mediated autophagy in tumors</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Pro-tumor</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B19-cells-08-01349" ref-type="bibr">19</xref>]</td></tr><tr><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>Epithelial mitophagy increases CD8+T-Cells</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Anti-tumor</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B34-cells-08-01349" ref-type="bibr">34</xref>]</td></tr><tr><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>Loss of PARK2 accelerates tumor development</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inactive</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Pro-tumor</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B38-cells-08-01349" ref-type="bibr">38</xref>]</td></tr><tr><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>Decreased ATG5 in CRC patients</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inactive</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Pro-tumor</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B73-cells-08-01349" ref-type="bibr">73</xref>]</td></tr><tr><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>Increased ATG5 yields increased invasion</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Pro-tumor</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B73-cells-08-01349" ref-type="bibr">73</xref>]</td></tr><tr><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>Active autophagy through LC3B and SQSTM1</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Pro-tumor</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B74-cells-08-01349" ref-type="bibr">74</xref>]</td></tr><tr><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>Loss of ATG7</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inactive</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Anti-tumor</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B75-cells-08-01349" ref-type="bibr">75</xref>]</td></tr><tr><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>RACK1 induces autophagy</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Pro-tumor</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B76-cells-08-01349" ref-type="bibr">76</xref>]</td></tr><tr><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>High Beclin-1 in CRC</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Pro-tumor</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B80-cells-08-01349" ref-type="bibr">80</xref>]</td></tr><tr><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>Increased LC3 with loss of p53</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Anti-tumor</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B81-cells-08-01349" ref-type="bibr">81</xref>]</td></tr><tr><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>Autophagy suppresses immune response in KRAS cancer</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Pro-tumor</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B82-cells-08-01349" ref-type="bibr">82</xref>]</td></tr><tr><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>Autophagy drives glycolysis in RAS cancers</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Pro-tumor</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B83-cells-08-01349" ref-type="bibr">83</xref>]</td></tr><tr><td colspan="5" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>B</bold></td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>Treatment</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>Autophagy</bold></td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1"><bold>Tumor response</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>Reference</bold></td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>Mito-CP or Mito-Met10</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1">Anti-Tumor; Decreased proliferation in KRAS mutant cancers.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B47-cells-08-01349" ref-type="bibr">47</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>BH3 mimetic and chloroquine</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inactive</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1">Anti-Tumor; Induced apoptosis.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B48-cells-08-01349" ref-type="bibr">48</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>Bafilomycin A1 or chloroquine</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inactive</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1">Anti-Tumor; Elevated FOXO3a and transcriptional upregulation of pro-apoptotic genes.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B77-cells-08-01349" ref-type="bibr">77</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>Brevlin A</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1">Anti-Tumor; Promoted expression of LC3-II and induced autophagy.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B79-cells-08-01349" ref-type="bibr">79</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>KRAS siRNA</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inactive</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1">Anti-Tumor; Inhibiting mutant Kras inhibits autophagy and induces apoptosis.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B84-cells-08-01349" ref-type="bibr">84</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>Vorinostat with chloroquine</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inactive</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1">Anti-Tumor; Induced apoptosis.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B85-cells-08-01349" ref-type="bibr">85</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>5-Fuorouracil and chloroquine</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inactive</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1">Anti-Tumor; 5-FU treatment induced autophagy for resistance. Inhibition of autophagy reduced growth.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B86-cells-08-01349" ref-type="bibr">86</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>Temsirolimus</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1">Anti-Tumor; Inhibited mTOR to activate autophagy and degrade CIP2A.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B87-cells-08-01349" ref-type="bibr">87</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>Estrogen Receptor Beta</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1">Anti-Tumor; Autophagy directed CyclinD1 degradation inhibited growth.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B88-cells-08-01349" ref-type="bibr">88</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><bold>4-Hydroxytamoxifen</bold></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Active</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin" rowspan="1">Anti-Tumor; Degradation of KRAS through autophagy induced cel death.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B89-cells-08-01349" ref-type="bibr">89</xref>]</td></tr></tbody></table></table-wrap></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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