CHOP过表达通过Bcl-2/JNK途径使人类非小细胞肺癌细胞对顺铂治疗敏感。
CHOP overexpression sensitizes human non-small cell lung cancer cells to cisplatin treatment by Bcl-2/JNK pathway.
作者信息
Wang Li-Le, Hu Rui-Cheng, Dai Ai-Guo, Tan Shuang-Xiang, Xu Ming, Kong Chun-Chu, Chen Yun-Rong, Fu Dai-Yan
机构信息
Department of Respiratory Medicine, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University Changsha 410016, China.
Department of Respiratory Diseases, Medical School, Hunan University of Chinese Medicine Changsha 410208, China.
出版信息
Am J Transl Res. 2021 Jun 15;13(6):6279-6287. eCollection 2021.
C/EBP homologous protein (CHOP), a 29 kDa cellular protein, plays a role in regulating tumor proliferation, differentiation, metabolism, cell death, and in tumor resistance to chemotherapy. Non-small cell lung cancer (NSCLC) is a tumor of the respiratory system and drug resistance is prevalent among NSCLC clinical cell cultures. Herein, our study elucidated the effect of CHOP on NSCLC cells with cisplatin resistance and its mechanism. In a NSCLC cell line with cisplatin-resistance, CHOP expression was decreased, compared with A549 cells. Overexpression of CHOP decreased the cell viability and enhanced cell apoptosis in the cells treated with cisplatin. Expression of CHOP also inhibited the cell proliferation and metastasis. CHOP increased the therapeutic effect of cisplatin on NSCLC cells through the Bcl-2/JNK pathway. In summary, CHOP regulated cisplatin resistance in cells of NSCLC by promoting the expression of apoptotic proteins and inhibiting the Bcl-2/JNK signaling pathway, indicating the antitumor effects of CHOP.
C/EBP 同源蛋白（CHOP）是一种 29 kDa 的细胞蛋白，在调节肿瘤增殖、分化、代谢、细胞死亡以及肿瘤对化疗的抗性方面发挥作用。非小细胞肺癌（NSCLC）是一种呼吸系统肿瘤，耐药性在 NSCLC 临床细胞培养物中普遍存在。在此，我们的研究阐明了 CHOP 对顺铂耐药的 NSCLC 细胞的影响及其机制。与 A549 细胞相比，在一株具有顺铂耐药性的 NSCLC 细胞系中，CHOP 的表达降低。CHOP 的过表达降低了用顺铂处理的细胞的活力并增强了细胞凋亡。CHOP 的表达还抑制了细胞增殖和转移。CHOP 通过 Bcl-2/JNK 途径增强了顺铂对 NSCLC 细胞的治疗效果。总之，CHOP 通过促进凋亡蛋白的表达和抑制 Bcl-2/JNK 信号通路来调节 NSCLC 细胞中的顺铂耐药性，表明了 CHOP 的抗肿瘤作用。
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