c-FLIP promotes drug resistance in non-small-cell lung cancer cells via upregulating FoxM1 expression

The forkhead box M1 (FoxM1) protein, a transcription factor, plays critical roles in regulating tumor growth and drug resistance, while cellular FLICE-inhibitory protein (c-FLIP), an anti-apoptotic regulator, is involved in the ubiquitin–proteasome pathway. In this study, we investigated the effects...

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Veröffentlicht in:	Acta pharmacologica Sinica 2022-11, Vol.43 (11), p.2956-2966
Hauptverfasser:	Wang, Wen-die, Shang, Yue, Wang, Chen, Ni, Jun, Wang, Ai-min, Li, Gao-jie, Su, Ling, Chen, Shu-zhen
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Apoptosis Biomedical and Life Sciences Biomedicine c-FLIP protein Carcinoma, Non-Small-Cell Lung - drug therapy Carcinoma, Non-Small-Cell Lung - metabolism CASP8 and FADD-Like Apoptosis Regulating Protein - genetics CASP8 and FADD-Like Apoptosis Regulating Protein - metabolism Cell Line, Tumor Cell Proliferation Drug resistance Drug Resistance, Neoplasm - genetics FLICE-inhibitory protein FLIP protein Forkhead Box Protein M1 - genetics Forkhead Box Protein M1 - metabolism Forkhead protein Forkhead Transcription Factors - metabolism Gene Expression Regulation, Neoplastic Humans Immunology Internal Medicine Lung cancer Lung Neoplasms - drug therapy Lung Neoplasms - metabolism Medical Microbiology Medical prognosis Mice Non-small cell lung carcinoma Pharmacology/Toxicology Post-transcription Proteasomes Small cell lung carcinoma Targeted cancer therapy Thiostrepton Thiostrepton - metabolism Thiostrepton - pharmacology Thiostrepton - therapeutic use Tumors Ubiquitin Ubiquitination Vaccine Xenografts β-Catenin
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Zusammenfassung:	The forkhead box M1 (FoxM1) protein, a transcription factor, plays critical roles in regulating tumor growth and drug resistance, while cellular FLICE-inhibitory protein (c-FLIP), an anti-apoptotic regulator, is involved in the ubiquitin–proteasome pathway. In this study, we investigated the effects of c-FLIP on the expression and ubiquitination levels of FoxM1 along with drug susceptibility in non-small-cell lung cancer (NSCLC) cells. We first showed that the expression levels of FoxM1 and c-FLIP were increased and positively correlated ( R 2 = 0.1106, P
ISSN:	1671-4083 1745-7254 1745-7254
DOI:	10.1038/s41401-022-00905-7