Opportunities and challenges of co-targeting epidermal growth factor receptor and autophagy signaling in non-small cell lung cancer
Identifieur interne : 000860 ( Pmc/Corpus ); 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 ; Wenxin Li ; Ni Zhang ; Xiaoli Zheng ; Zhao JingSource :
- 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
Links to Exploration step
PMC:6546992Le document en format XML
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<author><name sortKey="Wang, Xiaoju" sort="Wang, Xiaoju" uniqKey="Wang X" first="Xiaoju" last="Wang">Xiaoju Wang</name>
<affiliation><nlm:aff id="af1-ol-0-0-10372">Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, P.R. China</nlm:aff>
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<author><name sortKey="Li, Wenxin" sort="Li, Wenxin" uniqKey="Li W" first="Wenxin" last="Li">Wenxin Li</name>
<affiliation><nlm:aff id="af1-ol-0-0-10372">Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, P.R. China</nlm:aff>
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<author><name sortKey="Zhang, Ni" sort="Zhang, Ni" uniqKey="Zhang N" first="Ni" last="Zhang">Ni Zhang</name>
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<author><name sortKey="Zheng, Xiaoli" sort="Zheng, Xiaoli" uniqKey="Zheng X" first="Xiaoli" last="Zheng">Xiaoli Zheng</name>
<affiliation><nlm:aff id="af2-ol-0-0-10372">Cancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, P.R. China</nlm:aff>
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<author><name sortKey="Jing, Zhao" sort="Jing, Zhao" uniqKey="Jing Z" first="Zhao" last="Jing">Zhao Jing</name>
<affiliation><nlm:aff id="af1-ol-0-0-10372">Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, P.R. China</nlm:aff>
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<author><name sortKey="Li, Wenxin" sort="Li, Wenxin" uniqKey="Li W" first="Wenxin" last="Li">Wenxin Li</name>
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<author><name sortKey="Zheng, Xiaoli" sort="Zheng, Xiaoli" uniqKey="Zheng X" first="Xiaoli" last="Zheng">Xiaoli Zheng</name>
<affiliation><nlm:aff id="af2-ol-0-0-10372">Cancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, P.R. China</nlm:aff>
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<series><title level="j">Oncology Letters</title>
<idno type="ISSN">1792-1074</idno>
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<imprint><date when="2019">2019</date>
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<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>
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<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>
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<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>
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<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>
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<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>
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<pmc-comment> PMC Release delay is 0 months and 0 days and was based on the . </pmc-comment>
<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>
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