Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Nuclear protein 1 promotes unfolded protein response during endoplasmic reticulum stress, and alleviates apoptosis induced by cisplatin in non-small cell lung cancer cells

Yinhui Sun¹, Lihuai Wang² , Changqing Deng³, Hua Liu², Zhongcong Guo², Zelin Chang³, Jianxiong Mo³

¹Medical College, Hunan University of Traditional Chinese Medicine, Changsha City; ²Department of Oncology, The First Affiliated Hospital of Hunan University of Traditional Chinese Medicine, Changsha City; ³Department of Oncology, Hunan University of Traditional Chinese Medicine, Changsha City, Hunan Province 410000, China.

For correspondence:- Lihuai Wang Email: wanglihuai123@163.com Tel:+8673185369913

Accepted: 24 February 2021 Published: 31 March 2021

Citation: Sun Y, Wang L, Deng C, Liu H, Guo Z, Chang Z, et al. Nuclear protein 1 promotes unfolded protein response during endoplasmic reticulum stress, and alleviates apoptosis induced by cisplatin in non-small cell lung cancer cells. Trop J Pharm Res 2021; 20(3):519-524 doi: 10.4314/tjpr.v20i3.11

© 2021 The authors.
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Abstract

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.

Keywords: Non-small cell lung cancer (NSCLC), Nuclear protein 1 (NUPR1), unfolded protein response (UPR), Cisplatin, Endoplasmic reticulum (ER) stress