Department of Oncology, The General Hospital of Western Theater Command, Chengdu, Sichuan 610083, P.R. China.
Mol Med Rep. 2020 Oct;22(4):2966-2972. doi: 10.3892/mmr.2020.11349. Epub 2020 Jul 20.
Multidrug resistance of non‑small cell lung cancer (NSCLC) is a common clinical problem, which is one of the main reasons leading to the failure of chemotherapy. Therefore, how to overcome or prevent drug resistance has become a hot and difficult issue in clinical research. The present study was designed to investigate the expression patterns, functions and underlying mechanisms of MUC1 in regulating paclitaxel‑resistant cell line A549/PR in NSCLC. RT‑qPCR and western blot was performed to determine the mRNA and protein level, respectively. CCK‑8 was conducted to determine the cell viability of A549/PR cells. Moreover, flow cytometry assay was applied to examine the apoptosis rate of A549/PR. Herein, the MUC1 was over‑expressed in clinic NSCLC tissues and A549/PR cells. Silence of MUC1 could obviously suppress the proliferation and promote apoptosis of A549/PR cells in treatment of paclitaxel through up‑regulating the expression of Bax and Caspase‑3, and down‑regulating the expression of Bcl‑2, suggesting that chemotherapy combined with the modulation of MUC1 might be characterized as a promising therapeutic approach to overcome paclitaxel‑resistance in NSCLC in the future.
多药耐药性非小细胞肺癌（NSCLC）是一种常见的临床问题，是导致化疗失败的主要原因之一。因此，如何克服或预防耐药性已成为临床研究中的热点和难点问题。本研究旨在探讨 MUC1 在调节 NSCLC 紫杉醇耐药细胞系 A549/PR 中的表达模式、功能和潜在机制。通过 RT-qPCR 和 Western blot 分别测定 mRNA 和蛋白水平。CCK-8 测定 A549/PR 细胞的细胞活力。此外，通过流式细胞术检测 A549/PR 细胞的凋亡率。在此，MUC1 在临床 NSCLC 组织和 A549/PR 细胞中过表达。沉默 MUC1 通过上调 Bax 和 Caspase-3 的表达，下调 Bcl-2 的表达，明显抑制紫杉醇治疗后 A549/PR 细胞的增殖并促进其凋亡，提示化疗联合 MUC1 的调节可能是克服 NSCLC 紫杉醇耐药的一种很有前途的治疗方法。
