Gossypol overcomes EGFR-TKIs resistance in non-small cell lung cancer cells by targeting YAP/TAZ and EGFR
- Resource Type
- Authors
- Jian, Xu; Guo-Yuan, Zhu; Dai, Cao; Hao, Pan; Ying-Wei, Li
- Source
- Biomedicinepharmacotherapy = Biomedecinepharmacotherapie. 115
- Subject
- Caspase 7
Caspase 3
Contraceptive Agents, Male
Gossypol
Mice, Nude
Apoptosis
YAP-Signaling Proteins
ErbB Receptors
Gene Expression Regulation, Neoplastic
Drug Resistance, Neoplasm
Carcinoma, Non-Small-Cell Lung
Cell Line, Tumor
Gene Knockdown Techniques
Mutation
Animals
Humans
Protein Kinase Inhibitors
Acyltransferases
Adaptor Proteins, Signal Transducing
Cell Proliferation
Transcription Factors
- Language
- ISSN
- 1950-6007
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 EGFR