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• W2943041569 endingPage "108860" @default.
• W2943041569 startingPage "108860" @default.
• W2943041569 abstract "EGFR tyrosine kinase inhibitors (EGFR-TKIs) improve the progression-free survival of patients with non-small cell lung cancer (NSCLC). However, most patients inevitably developed drug resistance. EGFR T790 M mutation is the major mechanism for resistance to EGFR-TKIs and becomes an obstacle for the treatment of NSCLC patients with EGFR activating mutations. Besides, YAP/TAZ also confers resistance to EGFR-TKIs. Our previous study identified gossypol as a YAP/TAZ inhibitor. In the current study, we found that gossypol inhibited cell growth and induced apoptosis in H1975 cells harboring EGFRL858R/T790M. Also, gossypol treatment sensitized H1975 cells to EGFR-TKIs. Our mechanism studies showed that gossypol decreased the protein level of YAP/TAZ, which was abrogated by the proteasome inhibition. Moreover, over-expression of YAP/TAZ reversed the effects of gossypol on H1975 cells, and YAP/TAZ knockdown sensitized H1975 cells to gossypol treatment. Furthermore, gossypol reduced the protein level of EGFRL858R/T790M and inhibited the downstream ERK1/2 pathway in H1975 cells. Our findings suggested that gossypol might serve a promise drug candidate for overcoming EGFR-TKIs resistance by targeting both YAP/TAZ and EGFRL858R/T790M." @default.
• W2943041569 created "2019-05-09" @default.
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• W2943041569 date "2019-07-01" @default.
• W2943041569 modified "2023-09-30" @default.
• W2943041569 title "Gossypol overcomes EGFR-TKIs resistance in non-small cell lung cancer cells by targeting YAP/TAZ and EGFRL858R/T790M" @default.
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• W2943041569 doi "https://doi.org/10.1016/j.biopha.2019.108860" @default.
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