BCLAF1 induces cisplatin resistance in lung cancer cells
- Tao Jiang
- Bingjie Liu
- Dongping Wu
- Feng Zhang
Affiliations: College of Life Sciences, Shanghai Normal University, Shanghai 200234, P.R. China, Department of Radiation Oncology, Shaoxing People's Hospital, Shaoxing Hospital of Zhejiang University, Shaoxing, Zhejiang 312000, P.R. China
- Published online on: September 11, 2020 https://doi.org/10.3892/ol.2020.12090
Copyright: © Jiang
et al. This is an open access article distributed under the
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Treatment for non‑small cell lung cancer (NSCLC) remains challenging due to frequent recurrence and the development of resistance to platinum‑based chemotherapy. The mechanism underlying NSCLC chemoresistance remains unclear. The present study aimed to investigate the mechanism of cisplatin resistance in NSCLC cells and it found that the expression of Bcl‑2‑associated transcription factor 1 (BCLAF1) was higher in the A549 cell line with cisplatin resistance (A549/DDP) by western blotting and reverse‑transcription quantitative PCR, suggesting that elevated BCLAF1 expression is associated with acquired cisplatin resistance in A549 cells. BCLAF1 was found to promote DNA damage repair in A549/DDP cells by regulating γH2A histone family member X foci formation by immunofluorescence and western blotting. BCLAF1 was also demonstrated to regulate ubiquitin‑specific peptidase 22 mRNA expression in A549/DDP cells, in addition to regulating G1 phase arrest by targeting p21 expression. Taken together, these findings suggest that BCLAF1 mediates cisplatin resistance by regulating the repair of DNA damage and p21‑mediated G1 phase arrest.