Opportunities and challenges of co-targeting epidermal growth factor receptor and autophagy signaling in non-small cell lung cancer
Identifieur interne : 000860 ( Pmc/Curation ); précédent : 000859; suivant : 000861Opportunities and challenges of co-targeting epidermal growth factor receptor and autophagy signaling in non-small cell lung cancer
Auteurs : Xiaoju Wang [République populaire de Chine] ; Wenxin Li [République populaire de Chine] ; Ni Zhang [République populaire de Chine] ; Xiaoli Zheng [République populaire de Chine] ; Zhao Jing [République populaire de Chine]Source :
- Oncology Letters [ 1792-1074 ] ; 2019.
Abstract
Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are a standard therapy for patients with non-small cell lung cancer (NSCLC) with sensitive mutations. However, acquired resistance emerges following a median of 6–12 months. Several studies demonstrated that EGFR-TKI-induced tumor microenvironment stresses and autophagy are important causes of resistance. The current review summarizes the molecular mechanisms involved in EGFR-mediated regulation of autophagy. The role of autophagy in EGFR-TKI treatment, which may serve a role in protection or cell death, was discussed. Furthermore, co-inhibiting EGFR and autophagy signaling as a rational therapeutic strategy in the treatment of patients with NSCLC was explored.
Url:
DOI: 10.3892/ol.2019.10372
PubMed: 31289521
PubMed Central: 6546992
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China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002</wicri:regionArea></affiliation></author><author><name sortKey="Li, Wenxin" sort="Li, Wenxin" uniqKey="Li W" first="Wenxin" last="Li">Wenxin Li</name><affiliation wicri:level="1"><nlm:aff id="af1-ol-0-0-10372">Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002</wicri:regionArea></affiliation></author><author><name sortKey="Zhang, Ni" sort="Zhang, Ni" uniqKey="Zhang N" first="Ni" last="Zhang">Ni Zhang</name><affiliation wicri:level="1"><nlm:aff id="af1-ol-0-0-10372">Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002</wicri:regionArea></affiliation></author><author><name sortKey="Zheng, Xiaoli" sort="Zheng, Xiaoli" uniqKey="Zheng X" first="Xiaoli" last="Zheng">Xiaoli Zheng</name><affiliation wicri:level="1"><nlm:aff id="af2-ol-0-0-10372">Cancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Cancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002</wicri:regionArea></affiliation></author><author><name sortKey="Jing, Zhao" sort="Jing, Zhao" uniqKey="Jing Z" first="Zhao" last="Jing">Zhao Jing</name><affiliation wicri:level="1"><nlm:aff id="af1-ol-0-0-10372">Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002</wicri:regionArea></affiliation></author></analytic><series><title level="j">Oncology Letters</title><idno type="ISSN">1792-1074</idno><idno type="eISSN">1792-1082</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>Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are a standard therapy for patients with non-small cell lung cancer (NSCLC) with sensitive mutations. However, acquired resistance emerges following a median of 6–12 months. Several studies demonstrated that EGFR-TKI-induced tumor microenvironment stresses and autophagy are important causes of resistance. The current review summarizes the molecular mechanisms involved in EGFR-mediated regulation of autophagy. The role of autophagy in EGFR-TKI treatment, which may serve a role in protection or cell death, was discussed. Furthermore, co-inhibiting EGFR and autophagy signaling as a rational therapeutic strategy in the treatment of patients with NSCLC was explored.</p></div></front></TEI><pmc article-type="review-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Oncol Lett</journal-id><journal-id journal-id-type="iso-abbrev">Oncol Lett</journal-id><journal-id journal-id-type="publisher-id">OL</journal-id><journal-title-group><journal-title>Oncology Letters</journal-title></journal-title-group><issn pub-type="ppub">1792-1074</issn><issn pub-type="epub">1792-1082</issn><publisher><publisher-name>D.A. Spandidos</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31289521</article-id><article-id pub-id-type="pmc">6546992</article-id><article-id pub-id-type="doi">10.3892/ol.2019.10372</article-id><article-id pub-id-type="publisher-id">OL-0-0-10372</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Opportunities and challenges of co-targeting epidermal growth factor receptor and autophagy signaling in non-small cell lung cancer</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Xiaoju</given-names></name><xref ref-type="aff" rid="af1-ol-0-0-10372">1</xref></contrib><contrib contrib-type="author"><name><surname>Li</surname><given-names>Wenxin</given-names></name><xref ref-type="aff" rid="af1-ol-0-0-10372">1</xref></contrib><contrib contrib-type="author"><name><surname>Zhang</surname><given-names>Ni</given-names></name><xref ref-type="aff" rid="af1-ol-0-0-10372">1</xref></contrib><contrib contrib-type="author"><name><surname>Zheng</surname><given-names>Xiaoli</given-names></name><xref ref-type="aff" rid="af2-ol-0-0-10372">2</xref></contrib><contrib contrib-type="author"><name><surname>Jing</surname><given-names>Zhao</given-names></name><xref ref-type="aff" rid="af1-ol-0-0-10372">1</xref><xref rid="c1-ol-0-0-10372" ref-type="corresp"></xref></contrib></contrib-group><aff id="af1-ol-0-0-10372"><label>1</label>Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, P.R. China</aff><aff id="af2-ol-0-0-10372"><label>2</label>Cancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, P.R. China</aff><author-notes><corresp id="c1-ol-0-0-10372"><italic>Correspondence to</italic>: Dr Zhao Jing, Department of Radiation Oncology, Hangzhou Cancer Hospital, 34 Yanguan Lane, Hangzhou, Zhejiang 310002, P.R. China, E-mail: <email>jz96329@163.com</email></corresp></author-notes><pub-date pub-type="ppub"><month>7</month><year>2019</year></pub-date><pub-date pub-type="epub"><day>20</day><month>5</month><year>2019</year></pub-date><pub-date pub-type="pmc-release"><day>20</day><month>5</month><year>2019</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
<volume>18</volume><issue>1</issue><fpage>499</fpage><lpage>506</lpage><history><date date-type="received"><day>25</day><month>8</month><year>2018</year></date><date date-type="accepted"><day>11</day><month>4</month><year>2019</year></date></history><permissions><copyright-statement>Copyright © 2019, Spandidos Publications</copyright-statement><copyright-year>2019</copyright-year></permissions><abstract><p>Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are a standard therapy for patients with non-small cell lung cancer (NSCLC) with sensitive mutations. However, acquired resistance emerges following a median of 6–12 months. Several studies demonstrated that EGFR-TKI-induced tumor microenvironment stresses and autophagy are important causes of resistance. The current review summarizes the molecular mechanisms involved in EGFR-mediated regulation of autophagy. The role of autophagy in EGFR-TKI treatment, which may serve a role in protection or cell death, was discussed. Furthermore, co-inhibiting EGFR and autophagy signaling as a rational therapeutic strategy in the treatment of patients with NSCLC was explored.</p></abstract><kwd-group><kwd>epidermal growth factor receptor</kwd><kwd>autophagy</kwd><kwd>non-small-cell lung cancer</kwd><kwd>resistance</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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