Open AccessNuclear protein 1 promotes unfolded protein response during endoplasmic reticulum stress, and alleviates apoptosis induced by cisplatin in non-small cell lung cancer cells
Author(s) -
Yifeng Sun,
Lihuai Wang,
Chao Deng,
Hua Liu,
Zhongcong Guo,
Zelin Chang,
Jian-Xiong Mo
Publication year - 2022
Publication title -
tropical journal of pharmaceutical research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.209
H-Index - 36
eISSN - 1596-5996
pISSN - 1596-9827
DOI - 10.4314/tjpr.v20i3.11
Subject(s) - unfolded protein response , cisplatin , tunicamycin , endoplasmic reticulum , apoptosis , flow cytometry , chemistry , gene knockdown , cancer research , microbiology and biotechnology , biology , medicine , chemotherapy , biochemistry
Purpose: To investigate the role of nuclear protein 1 (NUPR1) in the drug resistance of non-small cell lung cancer (NSCLC) and its regulatory mechanisms.
Methods: Quantitative polymerase chain reaction (qPCR) and immunoblot assays were conducted to determine NUPR1 expression in A549 cells. Cisplatin sensitivity and cisplatin-induced apoptosis were investigated in NUPR1 knockdown or overexpressed cells via 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay and flow cytometry. The potential association between unfolded protein response (UPR) and NUPR1 levels in response to cisplatin were explored. The effect of endoplasmic reticulum (ER) stress on apoptosis was examined using flow cytometry.
Results: Cisplatin treatment promoted the expression of NUPR1 in NSCLC cells. NUPR1 regulated cisplatin resistance in NSCLC and also regulated UPR in ER stress induced by cisplatin. The results show NUPR1 regulated apoptosis induced by ER stress following tunicamycin treatment.
Conclusion: NSCLC cells may promote the UPR in ER stress by promoting the expression of NUPR1, thereby reducing the ER stress induced by cisplatin.