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RING finger protein 38 induces the drug resistance of cisplatin in non‐small‐cell lung cancer
Author(s) -
Wu Chao,
Chen Lei,
Tao Haitao,
Kong Lu,
Hu Yi
Publication year - 2021
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11423
Subject(s) - cisplatin , lung cancer , apoptosis , a549 cell , cancer research , gene silencing , viability assay , cell , blot , cell growth , cell culture , drug resistance , chemistry , biology , oncology , medicine , chemotherapy , biochemistry , gene , microbiology and biotechnology , genetics
Cisplatin resistance of non‐small‐cell lung cancer (NSCLC) needs to be well elucidated. RING finger protein (RNF38) has been proposed as a biomarker of NSCLC poor prognosis. However, its role in drug resistance in NSCLC is poorly understood. RNF38 expression was detected in normal lung epithelial cell and four NSCLC cell lines. RNF38 was stably overexpressed in A549 and H460 cells or silenced in H1975 and cisplatin‐resistant A549 cells (A549‐CDDP resistant) using lentiviral vectors. RNF38 expression levels were determined using quantitative real‐time polymerase chain reaction and western blotting analysis. Cell viability in response to different concentrations of cisplatin was evaluated by Cell Counting Kit‐8 assay. RNF38 expression levels were markedly elevated in NSCLC cells and cells harboring high RNF38 were less sensitive to cisplatin. Overexpression of RNF38 reduced, while RNF38 silencing increased the drug sensitivity of cisplatin in NSCLC cells. Cisplatin‐resistant cells expressed high RNF38 level. RNF38 silencing promoted cell apoptosis and enhanced the drug sensitivity of cisplatin in cisplatin‐resistant NSCLC cells. These findings indicate that RNF38 might induce cisplatin resistance of NSCLC cells via promoting cell apoptosis and RNF38 could be a novel target for rectify cisplatin resistance in NSCLC cases.