Adapting and Surviving: Intra and Extra-Cellular Remodeling in Drug-Resistant Gastric Cancer Cells
Identifieur interne : 000A21 ( Pmc/Curation ); précédent : 000A20; suivant : 000A22Adapting and Surviving: Intra and Extra-Cellular Remodeling in Drug-Resistant Gastric Cancer Cells
Auteurs : Sabino Russi [Italie] ; Henu Kumar Verma [Italie] ; Simona Laurino [Italie] ; Pellegrino Mazzone [Italie] ; Giovanni Storto [Italie] ; Anna Nardelli [Italie] ; Pietro Zoppoli [Italie] ; Giovanni Calice [Italie] ; Francesco La Rocca [Italie] ; Alessandro Sgambato [Italie] ; Valeria Lucci [Italie] ; Geppino Falco [Italie] ; Vitalba Ruggieri [Italie]Source :
- International Journal of Molecular Sciences [ 1422-0067 ] ; 2019.
Abstract
Despite the significant recent advances in clinical practice, gastric cancer (GC) represents a leading cause of cancer-related deaths in the world. In fact, occurrence of chemo-resistance still remains a daunting hindrance to effectiveness of the current approach to GC therapy. There is accumulating evidence that a plethora of cellular and molecular factors is implicated in drug-induced phenotypical switching of GC cells. Among them, epithelial-mesenchymal transition (EMT), autophagy, drug detoxification, DNA damage response and drug target alterations, have been reported as major determinants. Intriguingly, resistant GC phenotype may be the result of GC cell-induced tumor microenvironment (TME) remodeling, which is currently emerging as a key player in promoting drug resistance and overcoming cytotoxic effects of drugs. In this review, we discuss the possible mechanisms of drug resistance and their involvement in determining current GC therapies failure.
Url:
DOI: 10.3390/ijms20153736
PubMed: 31370155
PubMed Central: 6695752
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<front><div type="abstract" xml:lang="en"><p>Despite the significant recent advances in clinical practice, gastric cancer (GC) represents a leading cause of cancer-related deaths in the world. In fact, occurrence of chemo-resistance still remains a daunting hindrance to effectiveness of the current approach to GC therapy. There is accumulating evidence that a plethora of cellular and molecular factors is implicated in drug-induced phenotypical switching of GC cells. Among them, epithelial-mesenchymal transition (EMT), autophagy, drug detoxification, DNA damage response and drug target alterations, have been reported as major determinants. Intriguingly, resistant GC phenotype may be the result of GC cell-induced tumor microenvironment (TME) remodeling, which is currently emerging as a key player in promoting drug resistance and overcoming cytotoxic effects of drugs. In this review, we discuss the possible mechanisms of drug resistance and their involvement in determining current GC therapies failure.</p>
</div>
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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">Int J Mol Sci</journal-id>
<journal-id journal-id-type="iso-abbrev">Int J Mol Sci</journal-id>
<journal-id journal-id-type="publisher-id">ijms</journal-id>
<journal-title-group><journal-title>International Journal of Molecular Sciences</journal-title>
</journal-title-group>
<issn pub-type="epub">1422-0067</issn>
<publisher><publisher-name>MDPI</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31370155</article-id>
<article-id pub-id-type="pmc">6695752</article-id>
<article-id pub-id-type="doi">10.3390/ijms20153736</article-id>
<article-id pub-id-type="publisher-id">ijms-20-03736</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
</subj-group>
</article-categories>
<title-group><article-title>Adapting and Surviving: Intra and Extra-Cellular Remodeling in Drug-Resistant Gastric Cancer Cells</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0002-4467-4942</contrib-id>
<name><surname>Russi</surname>
<given-names>Sabino</given-names>
</name>
<xref ref-type="aff" rid="af1-ijms-20-03736">1</xref>
<xref ref-type="author-notes" rid="fn1-ijms-20-03736">†</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Verma</surname>
<given-names>Henu Kumar</given-names>
</name>
<xref ref-type="aff" rid="af2-ijms-20-03736">2</xref>
<xref ref-type="aff" rid="af3-ijms-20-03736">3</xref>
<xref ref-type="author-notes" rid="fn1-ijms-20-03736">†</xref>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0002-5220-3227</contrib-id>
<name><surname>Laurino</surname>
<given-names>Simona</given-names>
</name>
<xref ref-type="aff" rid="af1-ijms-20-03736">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Mazzone</surname>
<given-names>Pellegrino</given-names>
</name>
<xref ref-type="aff" rid="af3-ijms-20-03736">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Storto</surname>
<given-names>Giovanni</given-names>
</name>
<xref ref-type="aff" rid="af4-ijms-20-03736">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Nardelli</surname>
<given-names>Anna</given-names>
</name>
<xref ref-type="aff" rid="af5-ijms-20-03736">5</xref>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0002-7860-9655</contrib-id>
<name><surname>Zoppoli</surname>
<given-names>Pietro</given-names>
</name>
<xref ref-type="aff" rid="af1-ijms-20-03736">1</xref>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0002-2545-1401</contrib-id>
<name><surname>Calice</surname>
<given-names>Giovanni</given-names>
</name>
<xref ref-type="aff" rid="af1-ijms-20-03736">1</xref>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0002-8868-195X</contrib-id>
<name><surname>La Rocca</surname>
<given-names>Francesco</given-names>
</name>
<xref ref-type="aff" rid="af6-ijms-20-03736">6</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Sgambato</surname>
<given-names>Alessandro</given-names>
</name>
<xref ref-type="aff" rid="af7-ijms-20-03736">7</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Lucci</surname>
<given-names>Valeria</given-names>
</name>
<xref ref-type="aff" rid="af8-ijms-20-03736">8</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Falco</surname>
<given-names>Geppino</given-names>
</name>
<xref ref-type="aff" rid="af3-ijms-20-03736">3</xref>
<xref ref-type="aff" rid="af8-ijms-20-03736">8</xref>
<xref rid="c1-ijms-20-03736" ref-type="corresp">*</xref>
<xref ref-type="author-notes" rid="fn2-ijms-20-03736">‡</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ruggieri</surname>
<given-names>Vitalba</given-names>
</name>
<xref ref-type="aff" rid="af1-ijms-20-03736">1</xref>
<xref rid="c1-ijms-20-03736" ref-type="corresp">*</xref>
<xref ref-type="author-notes" rid="fn2-ijms-20-03736">‡</xref>
</contrib>
</contrib-group>
<aff id="af1-ijms-20-03736"><label>1</label>
Laboratory of Preclinical and Translational Research, IRCCS-Referral Cancer Center of Basilicata (CROB), 85028 Rionero in Vulture (PZ), Italy</aff>
<aff id="af2-ijms-20-03736"><label>2</label>
Institute of Experimental Endocrinology and Oncology, National Research Council, 80131 Naples, Italy</aff>
<aff id="af3-ijms-20-03736"><label>3</label>
Section of Stem Cell and Development, Istituto di Ricerche Genetiche “Gaetano Salvatore” Biogem s.c. a.r.l., 83031 Ariano Irpino, Italy</aff>
<aff id="af4-ijms-20-03736"><label>4</label>
Department of Nuclear Medicine, IRCCS—Referral Cancer Center of Basilicata (CROB), 85028 Rionero in Vulture (PZ), Italy</aff>
<aff id="af5-ijms-20-03736"><label>5</label>
Istituto di Biostrutture e Bioimmagini, Consiglio Nazionale delle Ricerche, 80145 Napoli, Italy</aff>
<aff id="af6-ijms-20-03736"><label>6</label>
Laboratory of Clinical Research and Advanced Diagnostics, IRCCS-Referral Cancer Center of Basilicata (CROB), 85028 Rionero in Vulture (PZ), Italy</aff>
<aff id="af7-ijms-20-03736"><label>7</label>
Scientific Direction, IRCCS-Referral Cancer Center of Basilicata (CROB), 85028 Rionero in Vulture (PZ), Italy</aff>
<aff id="af8-ijms-20-03736"><label>8</label>
Department of Biology, University of Naples Federico II, 80126 Naples, Italy</aff>
<author-notes><corresp id="c1-ijms-20-03736"><label>*</label>
Correspondence: <email>geppino.falco@unina.it</email>
(G.F.); <email>vitalba.ruggieri@crob.it</email>
(V.R.); Tel.: +39-081-679092 (G.F.); +39-0972-726239 (V.R.)</corresp>
<fn id="fn1-ijms-20-03736"><label>†</label>
<p>These authors contributed equally to this work.</p>
</fn>
<fn id="fn2-ijms-20-03736"><label>‡</label>
<p>Contributed equally as last authors.</p>
</fn>
</author-notes>
<pub-date pub-type="epub"><day>31</day>
<month>7</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection"><month>8</month>
<year>2019</year>
</pub-date>
<volume>20</volume>
<issue>15</issue>
<elocation-id>3736</elocation-id>
<history><date date-type="received"><day>03</day>
<month>7</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>29</day>
<month>7</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>Despite the significant recent advances in clinical practice, gastric cancer (GC) represents a leading cause of cancer-related deaths in the world. In fact, occurrence of chemo-resistance still remains a daunting hindrance to effectiveness of the current approach to GC therapy. There is accumulating evidence that a plethora of cellular and molecular factors is implicated in drug-induced phenotypical switching of GC cells. Among them, epithelial-mesenchymal transition (EMT), autophagy, drug detoxification, DNA damage response and drug target alterations, have been reported as major determinants. Intriguingly, resistant GC phenotype may be the result of GC cell-induced tumor microenvironment (TME) remodeling, which is currently emerging as a key player in promoting drug resistance and overcoming cytotoxic effects of drugs. In this review, we discuss the possible mechanisms of drug resistance and their involvement in determining current GC therapies failure.</p>
</abstract>
<kwd-group><kwd>gastric cancer</kwd>
<kwd>drug resistance</kwd>
<kwd>cellular reprogramming</kwd>
<kwd>cell behavior</kwd>
</kwd-group>
</article-meta>
</front>
<floats-group><fig id="ijms-20-03736-f001" orientation="portrait" position="float"><label>Figure 1</label>
<caption><p>Schematic representation of the most common mechanisms involved in chemo-resistance of gastric cancer (GC) cells. <bold>Angiogenesis:</bold>
hypoxia regulated genes and growth factors released by GC and cancer-associated fibroblasts (CAFs) implicated in chemo-resistance. <bold>Epithelial-Mesenchymal Transition (EMT):</bold>
factors involved in epithelial-mesenchymal switch that makes cancer cells drug-resistant and able to metastasize. <bold>Autophagy:</bold>
proteins involved in (1) isolation of cellular components for degradation in autophagosome, (2) fusion between autophagosome and lysosome, and (3) catabolic processes in autophagolysosome and found associated with chemo-resistance. <bold>Multidrug Resistance (MDR):</bold>
proteins involved in reduced drug uptake or increased drug efflux; increased drug detoxification; mutation or down-regulation of drug targets; up-regulation of drug targets; increased drug-induced DNA damage repair or telomere maintenance pathways; epigenetic regulation of gene expression. Abbreviations: solute carrier (SLC) and ATP-binding cassette (ABC) transporters; glutathione S-transferase (GST); Topo II (Topoisomerase II); thymidylate synthase (TS); DNA methyltransferases (DNMTs). (Images built with illustrations from <uri xlink:href="https://smart.servier.com">https://smart.servier.com</uri>
under CC 3.0 license).</p>
</caption>
<graphic xlink:href="ijms-20-03736-g001"></graphic>
</fig>
</floats-group>
</pmc>
</record>
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