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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Le document en format XML
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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>
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