Targeting Non-Oncogene Addiction: Focus on Thyroid Cancer
Identifieur interne : 000913 ( Pmc/Curation ); précédent : 000912; suivant : 000914Targeting Non-Oncogene Addiction: Focus on Thyroid Cancer
Auteurs : Maria Chiara Anania ; Tiziana Di Marco ; Mara Mazzoni ; Angela GrecoSource :
- Cancers [ 2072-6694 ] ; 2020.
Abstract
Thyroid carcinoma (TC) is the most common malignancy of endocrine organs with an increasing incidence in industrialized countries. The majority of TC are characterized by a good prognosis, even though cases with aggressive forms not cured by standard therapies are also present. Moreover, target therapies have led to low rates of partial response and prompted the emergence of resistance, indicating that new therapies are needed. In this review, we summarize current literature about the non-oncogene addiction (NOA) concept, which indicates that cancer cells, at variance with normal cells, rely on the activity of genes, usually not mutated or aberrantly expressed, essential for coping with the transformed phenotype. We highlight the potential of non-oncogenes as a point of intervention for cancer therapy in general, and present evidence for new putative non-oncogenes that are essential for TC survival and that may constitute attractive new therapeutic targets.
Url:
DOI: 10.3390/cancers12010129
PubMed: 31947935
PubMed Central: 7017043
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<author><name sortKey="Mazzoni, Mara" sort="Mazzoni, Mara" uniqKey="Mazzoni M" first="Mara" last="Mazzoni">Mara Mazzoni</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Targeting Non-Oncogene Addiction: Focus on Thyroid Cancer</title>
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<front><div type="abstract" xml:lang="en"><p>Thyroid carcinoma (TC) is the most common malignancy of endocrine organs with an increasing incidence in industrialized countries. The majority of TC are characterized by a good prognosis, even though cases with aggressive forms not cured by standard therapies are also present. Moreover, target therapies have led to low rates of partial response and prompted the emergence of resistance, indicating that new therapies are needed. In this review, we summarize current literature about the non-oncogene addiction (NOA) concept, which indicates that cancer cells, at variance with normal cells, rely on the activity of genes, usually not mutated or aberrantly expressed, essential for coping with the transformed phenotype. We highlight the potential of non-oncogenes as a point of intervention for cancer therapy in general, and present evidence for new putative non-oncogenes that are essential for TC survival and that may constitute attractive new therapeutic targets.</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">Cancers (Basel)</journal-id>
<journal-id journal-id-type="iso-abbrev">Cancers (Basel)</journal-id>
<journal-id journal-id-type="publisher-id">cancers</journal-id>
<journal-title-group><journal-title>Cancers</journal-title>
</journal-title-group>
<issn pub-type="epub">2072-6694</issn>
<publisher><publisher-name>MDPI</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31947935</article-id>
<article-id pub-id-type="pmc">7017043</article-id>
<article-id pub-id-type="doi">10.3390/cancers12010129</article-id>
<article-id pub-id-type="publisher-id">cancers-12-00129</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
</subj-group>
</article-categories>
<title-group><article-title>Targeting Non-Oncogene Addiction: Focus on Thyroid Cancer</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0003-4012-1870</contrib-id>
<name><surname>Anania</surname>
<given-names>Maria Chiara</given-names>
</name>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0001-9854-2657</contrib-id>
<name><surname>Di Marco</surname>
<given-names>Tiziana</given-names>
</name>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0001-6710-1410</contrib-id>
<name><surname>Mazzoni</surname>
<given-names>Mara</given-names>
</name>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0003-2994-0349</contrib-id>
<name><surname>Greco</surname>
<given-names>Angela</given-names>
</name>
<xref rid="c1-cancers-12-00129" ref-type="corresp">*</xref>
</contrib>
</contrib-group>
<aff id="af1-cancers-12-00129">Molecular Mechanisms Unit, Department of Research, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy;<email>mariachiara.anania@istitutotumori.mi.it</email>
(M.C.A.);<email>tiziana.dimarco@istitutotumori.mi.it</email>
(T.D.M.);<email>mara.mazzoni@istitutotumori.mi.it</email>
(M.M.)</aff>
<author-notes><corresp id="c1-cancers-12-00129"><label>*</label>
Correspondence: <email>angela.greco@istitutotumori.mi.it</email>
; Tel.: +39-0223903222</corresp>
</author-notes>
<pub-date pub-type="epub"><day>04</day>
<month>1</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="collection"><month>1</month>
<year>2020</year>
</pub-date>
<volume>12</volume>
<issue>1</issue>
<elocation-id>129</elocation-id>
<history><date date-type="received"><day>26</day>
<month>11</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>24</day>
<month>12</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>© 2020 by the authors.</copyright-statement>
<copyright-year>2020</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>Thyroid carcinoma (TC) is the most common malignancy of endocrine organs with an increasing incidence in industrialized countries. The majority of TC are characterized by a good prognosis, even though cases with aggressive forms not cured by standard therapies are also present. Moreover, target therapies have led to low rates of partial response and prompted the emergence of resistance, indicating that new therapies are needed. In this review, we summarize current literature about the non-oncogene addiction (NOA) concept, which indicates that cancer cells, at variance with normal cells, rely on the activity of genes, usually not mutated or aberrantly expressed, essential for coping with the transformed phenotype. We highlight the potential of non-oncogenes as a point of intervention for cancer therapy in general, and present evidence for new putative non-oncogenes that are essential for TC survival and that may constitute attractive new therapeutic targets.</p>
</abstract>
<kwd-group><kwd>non-oncogene addiction</kwd>
<kwd>thyroid cancer</kwd>
<kwd>functional screening</kwd>
<kwd>non-oncogenes</kwd>
<kwd>tumor vulnerabilities</kwd>
<kwd>therapeutic targets</kwd>
</kwd-group>
</article-meta>
</front>
<floats-group><fig id="cancers-12-00129-f001" orientation="portrait" position="float"><label>Figure 1</label>
<caption><p>Schematic representations of non-oncogene addictions (NOAs). Examples of stress support pathways to which tumor cells, but not normal cells, are addicted. Interfering with these pathways, which represent NOAs, can be selectively lethal for tumor cells. Figure created with BioRender.</p>
</caption>
<graphic xlink:href="cancers-12-00129-g001"></graphic>
</fig>
<fig id="cancers-12-00129-f002" orientation="portrait" position="float"><label>Figure 2</label>
<caption><p>Examples of RNA interference (RNAi) screening approaches. In vitro screening: libraries are directly screened in tumor and normal cells, used as a control <bold>(a)</bold>
; in vivo screening: libraries are directly injected in mice (<bold>b</bold>
), transfected in cells before transplantation (<bold>c</bold>
), or transfected in PDX (patient-derived xenograft)-derived cells (<bold>d</bold>
). For all the approaches, cells or tissues were analyzed for phenotypic alterations. Figure created with BioRender.</p>
</caption>
<graphic xlink:href="cancers-12-00129-g002"></graphic>
</fig>
<fig id="cancers-12-00129-f003" orientation="portrait" position="float"><label>Figure 3</label>
<caption><p>Scheme of therapeutic targets in thyroid tumor cells. Tyrosine kinase receptors, along with their downstream pathways, and pharmacological inhibitors entered in clinical practice are shown in gray; drugs, tested at pre-clinical and clinical level, targeting NOAs, are shown in red; the dotted lines represent putative NOAs whose inhibitor is not yet available. AICAR: 5-aminoimidazole-4-carboxamide-ribonucleoside; AKT: serine/threonine kinase 1; ALK: anaplastic lymphoma receptor tyrosine kinase; AMPK: adenosine monophosphate-activated protein kinase; ASCT: alanineserinecysteine-type amino acid transporter; CDK4/6: cyclin-dependent kinase 4/6; COPZ1: coatomer protein complex zeta 1; COX-2: cyclooxygenase-2; DUOX1: dual oxidase 1; Eph: ephrin; ERK: extracellular signal–regulated kinases; GLUT1: glucose transporter 1; G6PD: glucose-6-phosphate dehydrogenase; HDAC: histone deacetylase; HER2/3: erb-b2 receptor tyrosine kinase 2/3; HK1: hexokinase 1; HSP90: heat-shock protein 90; IGFR: insulin-like growth factor 1 receptor; LDHA: lactate dehydrogenase A; MASTL: microtubule associated serine/threonine kinase-like; MEK: mitogen-activated protein kinase; mTOR: mammalian target of rapamycin; NOX4: nicotinamide adenine dinucleotide phosphate NADPH oxidase 4; NSAID: nonsteroidal anti-inflammatory drug; PGE2: prostaglandine E2; PI3K: phosphatidylinositol-3-kinase; RAS: rat sarcoma viral oncogene homolog; RAF: rapidly accelerated fibrosarcoma; RET: rearranged during transfection; ROS: reactive oxygen species; TKT: transketolase; TRK: tropomyosin receptor kinase; VEGF: vascular endothelial growth factor; VEGFR: vascular endothelial growth factor receptor. Figure created with BioRender.</p>
</caption>
<graphic xlink:href="cancers-12-00129-g003"></graphic>
</fig>
</floats-group>
</pmc>
</record>
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