Opportunities and challenges of co-targeting epidermal growth factor receptor and autophagy signaling in non-small cell lung cancer
Identifieur interne : 000570 ( Main/Exploration ); précédent : 000569; suivant : 000571Opportunities 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
Affiliations:
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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><wicri:noRegion>Zhejiang 310002</wicri:noRegion></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. 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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><wicri:noRegion>Zhejiang 310002</wicri:noRegion></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><wicri:noRegion>Zhejiang 310002</wicri:noRegion></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><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wang, Xiaoju" sort="Wang, Xiaoju" uniqKey="Wang X" first="Xiaoju" last="Wang">Xiaoju Wang</name></noRegion><name sortKey="Jing, Zhao" sort="Jing, Zhao" uniqKey="Jing Z" first="Zhao" last="Jing">Zhao Jing</name><name sortKey="Li, Wenxin" sort="Li, Wenxin" uniqKey="Li W" first="Wenxin" last="Li">Wenxin Li</name><name sortKey="Zhang, Ni" sort="Zhang, Ni" uniqKey="Zhang N" first="Ni" last="Zhang">Ni Zhang</name><name sortKey="Zheng, Xiaoli" sort="Zheng, Xiaoli" uniqKey="Zheng X" first="Xiaoli" last="Zheng">Xiaoli Zheng</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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