Crosstalk between autophagy and epithelial-mesenchymal transition and its application in cancer therapy
Identifieur interne : 000245 ( Pmc/Curation ); précédent : 000244; suivant : 000246Crosstalk between autophagy and epithelial-mesenchymal transition and its application in cancer therapy
Auteurs : Hong-Tao Chen ; Hao Liu ; Min-Jie Mao ; Yuan Tan ; Xiang-Qiong Mo ; Xiao-Jun Meng ; Meng-Ting Cao ; Chu-Yu Zhong ; Yan Liu ; Hong Shan ; Guan-Min JiangSource :
- Molecular Cancer [ 1476-4598 ] ; 2019.
Abstract
Autophagy is a highly conserved catabolic process that mediates degradation of pernicious or dysfunctional cellular components, such as invasive pathogens, senescent proteins, and organelles. It can promote or suppress tumor development, so it is a “double-edged sword” in tumors that depends on the cell and tissue types and the stages of tumor. The epithelial-mesenchymal transition (EMT) is a complex biological trans-differentiation process that allows epithelial cells to transiently obtain mesenchymal features, including motility and metastatic potential. EMT is considered as an important contributor to the invasion and metastasis of cancers. Thus, clarifying the crosstalk between autophagy and EMT will provide novel targets for cancer therapy. It was reported that EMT-related signal pathways have an impact on autophagy; conversely, autophagy activation can suppress or strengthen EMT by regulating various signaling pathways. On one hand, autophagy activation provides energy and basic nutrients for EMT during metastatic spreading, which assists cells to survive in stressful environmental and intracellular conditions. On the other hand, autophagy, acting as a cancer-suppressive function, is inclined to hinder metastasis by selectively down-regulating critical transcription factors of EMT in the early phases. Therefore, the inhibition of EMT by autophagy inhibitors or activators might be a novel strategy that provides thought and enlightenment for the treatment of cancer. In this article, we discuss in detail the role of autophagy and EMT in the development of cancers, the regulatory mechanisms between autophagy and EMT, the effects of autophagy inhibition or activation on EMT, and the potential applications in anticancer therapy.
Url:
DOI: 10.1186/s12943-019-1030-2
PubMed: 31126310
PubMed Central: 6533683
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<front><div type="abstract" xml:lang="en"><p id="Par1">Autophagy is a highly conserved catabolic process that mediates degradation of pernicious or dysfunctional cellular components, such as invasive pathogens, senescent proteins, and organelles. It can promote or suppress tumor development, so it is a “double-edged sword” in tumors that depends on the cell and tissue types and the stages of tumor. The epithelial-mesenchymal transition (EMT) is a complex biological trans-differentiation process that allows epithelial cells to transiently obtain mesenchymal features, including motility and metastatic potential. EMT is considered as an important contributor to the invasion and metastasis of cancers. Thus, clarifying the crosstalk between autophagy and EMT will provide novel targets for cancer therapy. It was reported that EMT-related signal pathways have an impact on autophagy; conversely, autophagy activation can suppress or strengthen EMT by regulating various signaling pathways. On one hand, autophagy activation provides energy and basic nutrients for EMT during metastatic spreading, which assists cells to survive in stressful environmental and intracellular conditions. On the other hand, autophagy, acting as a cancer-suppressive function, is inclined to hinder metastasis by selectively down-regulating critical transcription factors of EMT in the early phases. Therefore, the inhibition of EMT by autophagy inhibitors or activators might be a novel strategy that provides thought and enlightenment for the treatment of cancer. In this article, we discuss in detail the role of autophagy and EMT in the development of cancers, the regulatory mechanisms between autophagy and EMT, the effects of autophagy inhibition or activation on EMT, and the potential applications in anticancer therapy.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Mol Cancer</journal-id>
<journal-id journal-id-type="iso-abbrev">Mol. Cancer</journal-id>
<journal-title-group><journal-title>Molecular Cancer</journal-title>
</journal-title-group>
<issn pub-type="epub">1476-4598</issn>
<publisher><publisher-name>BioMed Central</publisher-name>
<publisher-loc>London</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31126310</article-id>
<article-id pub-id-type="pmc">6533683</article-id>
<article-id pub-id-type="publisher-id">1030</article-id>
<article-id pub-id-type="doi">10.1186/s12943-019-1030-2</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
</subj-group>
</article-categories>
<title-group><article-title>Crosstalk between autophagy and epithelial-mesenchymal transition and its application in cancer therapy</article-title>
</title-group>
<contrib-group><contrib contrib-type="author" equal-contrib="yes"><name><surname>Chen</surname>
<given-names>Hong-Tao</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author" equal-contrib="yes"><name><surname>Liu</surname>
<given-names>Hao</given-names>
</name>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author" equal-contrib="yes"><name><surname>Mao</surname>
<given-names>Min-Jie</given-names>
</name>
<xref ref-type="aff" rid="Aff3">3</xref>
</contrib>
<contrib contrib-type="author" equal-contrib="yes"><name><surname>Tan</surname>
<given-names>Yuan</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Mo</surname>
<given-names>Xiang-Qiong</given-names>
</name>
<xref ref-type="aff" rid="Aff5">5</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Meng</surname>
<given-names>Xiao-Jun</given-names>
</name>
<xref ref-type="aff" rid="Aff6">6</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Cao</surname>
<given-names>Meng-Ting</given-names>
</name>
<xref ref-type="aff" rid="Aff7">7</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zhong</surname>
<given-names>Chu-Yu</given-names>
</name>
<xref ref-type="aff" rid="Aff8">8</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Liu</surname>
<given-names>Yan</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Shan</surname>
<given-names>Hong</given-names>
</name>
<address><email>shanhong@mail.sysu.edu.cn</email>
</address>
<xref ref-type="aff" rid="Aff9">9</xref>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Jiang</surname>
<given-names>Guan-Min</given-names>
</name>
<address><email>jianggm3@mail.sysu.edu.cn</email>
</address>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<aff id="Aff1"><label>1</label>
<institution-wrap><institution-id institution-id-type="GRID">grid.452859.7</institution-id>
<institution>Department of Clinical Laboratory,</institution>
<institution>The Fifth Affiliated Hospital of Sun Yat-sen University,</institution>
</institution-wrap>
Zhuhai, 2528000 Guangdong China</aff>
<aff id="Aff2"><label>2</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0000 8653 1072</institution-id>
<institution-id institution-id-type="GRID">grid.410737.6</institution-id>
<institution>Cancer Hospital and Cancer Research Institute, Guangzhou Medical University,</institution>
</institution-wrap>
Guangzhou, Guangdong China</aff>
<aff id="Aff3"><label>3</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1803 6191</institution-id>
<institution-id institution-id-type="GRID">grid.488530.2</institution-id>
<institution>Department of Laboratory Medicine, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine,</institution>
<institution>Sun Yat-sen University Cancer Center,</institution>
</institution-wrap>
Guangzhou, Guangdong China</aff>
<aff id="Aff4"><label>4</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0379 7164</institution-id>
<institution-id institution-id-type="GRID">grid.216417.7</institution-id>
<institution>Department of Clinical Laboratory, Hunan Cancer Hospital, The Affiliated Cancer Hospital of Xiangya School of Medicine,</institution>
<institution>Central South University,</institution>
</institution-wrap>
Changsha, Hunan China</aff>
<aff id="Aff5"><label>5</label>
<institution-wrap><institution-id institution-id-type="GRID">grid.452859.7</institution-id>
<institution>Department of Gastrointestinal Surgery,</institution>
<institution>The Fifth Affiliated Hospital of Sun Yat-sen University,</institution>
</institution-wrap>
Zhuhai, Guangdong China</aff>
<aff id="Aff6"><label>6</label>
<institution-wrap><institution-id institution-id-type="GRID">grid.452859.7</institution-id>
<institution>Department of Endocrinology,</institution>
<institution>The Fifth Affiliated Hospital of Sun Yat-sen University,</institution>
</institution-wrap>
Zhuhai, Guangdong China</aff>
<aff id="Aff7"><label>7</label>
<institution-wrap><institution-id institution-id-type="GRID">grid.461579.8</institution-id>
<institution>Department of Clinical Laboratory,</institution>
<institution>The First Affiliated Hospital of University of South China,</institution>
</institution-wrap>
Hengyang, Hunan China</aff>
<aff id="Aff8"><label>8</label>
<institution-wrap><institution-id institution-id-type="GRID">grid.452859.7</institution-id>
<institution>Department of Geriatrics,</institution>
<institution>The Fifth Affiliated Hospital of Sun Yat-sen University,</institution>
</institution-wrap>
Zhuhai, Guangdong China</aff>
<aff id="Aff9"><label>9</label>
<institution-wrap><institution-id institution-id-type="GRID">grid.452859.7</institution-id>
<institution>Guangdong Provincial Key Laboratory of Biomedical Imaging,</institution>
<institution>The Fifth Affiliated Hospital of Sun Yat-sen University,</institution>
</institution-wrap>
Zhuhai, 2528000 Guangdong China</aff>
</contrib-group>
<pub-date pub-type="epub"><day>24</day>
<month>5</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>24</day>
<month>5</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection"><year>2019</year>
</pub-date>
<volume>18</volume>
<elocation-id>101</elocation-id>
<history><date date-type="received"><day>24</day>
<month>3</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>15</day>
<month>5</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>© The Author(s). 2019</copyright-statement>
<license license-type="OpenAccess"><license-p><bold>Open Access</bold>
This article is distributed under the terms of the Creative Commons Attribution 4.0 International 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>
), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/publicdomain/zero/1.0/">http://creativecommons.org/publicdomain/zero/1.0/</ext-link>
) applies to the data made available in this article, unless otherwise stated.</license-p>
</license>
</permissions>
<abstract id="Abs1"><p id="Par1">Autophagy is a highly conserved catabolic process that mediates degradation of pernicious or dysfunctional cellular components, such as invasive pathogens, senescent proteins, and organelles. It can promote or suppress tumor development, so it is a “double-edged sword” in tumors that depends on the cell and tissue types and the stages of tumor. The epithelial-mesenchymal transition (EMT) is a complex biological trans-differentiation process that allows epithelial cells to transiently obtain mesenchymal features, including motility and metastatic potential. EMT is considered as an important contributor to the invasion and metastasis of cancers. Thus, clarifying the crosstalk between autophagy and EMT will provide novel targets for cancer therapy. It was reported that EMT-related signal pathways have an impact on autophagy; conversely, autophagy activation can suppress or strengthen EMT by regulating various signaling pathways. On one hand, autophagy activation provides energy and basic nutrients for EMT during metastatic spreading, which assists cells to survive in stressful environmental and intracellular conditions. On the other hand, autophagy, acting as a cancer-suppressive function, is inclined to hinder metastasis by selectively down-regulating critical transcription factors of EMT in the early phases. Therefore, the inhibition of EMT by autophagy inhibitors or activators might be a novel strategy that provides thought and enlightenment for the treatment of cancer. In this article, we discuss in detail the role of autophagy and EMT in the development of cancers, the regulatory mechanisms between autophagy and EMT, the effects of autophagy inhibition or activation on EMT, and the potential applications in anticancer therapy.</p>
</abstract>
<kwd-group xml:lang="en"><title>Keywords</title>
<kwd>Autophagy</kwd>
<kwd>Epithelial-mesenchymal transition</kwd>
<kwd>Cancer metastasis</kwd>
<kwd>Anticancer therapy</kwd>
</kwd-group>
<funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">http://dx.doi.org/10.13039/501100001809</institution-id>
<institution>National Natural Science Foundation of China</institution>
</institution-wrap>
</funding-source>
<award-id>81502104</award-id>
<award-id>81430041</award-id>
<award-id>81620108017</award-id>
<principal-award-recipient><name><surname>Shan</surname>
<given-names>Hong</given-names>
</name>
<name><surname>Jiang</surname>
<given-names>Guan-Min</given-names>
</name>
</principal-award-recipient>
</award-group>
</funding-group>
<funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">http://dx.doi.org/10.13039/501100010903</institution-id>
<institution>Key Programme</institution>
</institution-wrap>
</funding-source>
<award-id>2018YFC0910600</award-id>
<principal-award-recipient><name><surname>Shan</surname>
<given-names>Hong</given-names>
</name>
</principal-award-recipient>
</award-group>
</funding-group>
<funding-group><award-group><funding-source><institution> Hunan Young Talent</institution>
</funding-source>
<award-id>2017RS3051</award-id>
<principal-award-recipient><name><surname>Jiang</surname>
<given-names>Guan-Min</given-names>
</name>
</principal-award-recipient>
</award-group>
</funding-group>
<funding-group><award-group><funding-source><institution>Key Laboratory of Biomedical Imaging of Guangdong Province</institution>
</funding-source>
<award-id>2018B030322006</award-id>
<principal-award-recipient><name><surname>Shan</surname>
<given-names>Hong</given-names>
</name>
</principal-award-recipient>
</award-group>
</funding-group>
<custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name>
<meta-value>© The Author(s) 2019</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
</record>
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