Pulmonary Medicine Department (Inpatient Area 1), The Affiliated Cancer Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
Exp Lung Res. 2021 May-Jun;47(5):250-259. doi: 10.1080/01902148.2021.1916651. Epub 2021 Apr 24.
To delve into the related molecular mechanism of ACTL6A on non-small cell lung cancer (NSCLC) cell growth and apoptosis. Quantitative real-time polymerase chain reaction, immunohistochemical staining, and western blot assays were employed to examine ACTL6A mRNA and protein expression in four NSCLC cell line (NCI-H2170, LTEP-s, NCI-H1703, and PC-9) and normal lung cell line (BEAS-2B). CCK-8 cell viability assays and clone formation assay were applied to verify the cell proliferation of NCI-H2170 cell line after knockdown of ACTL6A. Flow cytometry assays were applied to check the role of ACTL6A in the apoptosis of NSCLC cells. The western blot assays were employed to examine the protein expression of WWC1, YAP, TAZ, and CYR61 in NCI-H2170 after knockdown of ACTL6A. Finally, xenograft tumor was taken out and checked the tumor volumes and weight. Immunohistochemical staining and western blot assays were employed to examine cell proliferation and apoptosis of NSCLC . In this study, the results showed that the mRNA and protein expression level of ACTL6A was higher in four NSCLC cell line than normal lung cell line, respectively. Suppression of ACTL6A inhibited the growth and promoted apoptosis of NSCLC cells. Meanwhile, ACTL6A promotes tumor growth and inhibits apoptosis of NSCLC via Hippo/YAP signaling pathway. ACTL6A promotes the proliferation in NSCLC by regulating Hippo/YAP pathway.
探讨 ACTL6A 对非小细胞肺癌（NSCLC）细胞生长和凋亡的相关分子机制。采用定量实时聚合酶链反应、免疫组织化学染色和 Western blot 检测 4 种 NSCLC 细胞系（NCI-H2170、LTEP-s、NCI-H1703 和 PC-9）和正常肺细胞系（BEAS-2B）中 ACTL6A mRNA 和蛋白的表达。CCK-8 细胞活力检测和克隆形成实验验证了 ACTL6A 敲低后 NCI-H2170 细胞系的细胞增殖。流式细胞术检测 ACTL6A 在 NSCLC 细胞凋亡中的作用。Western blot 检测 ACTL6A 敲低后 NCI-H2170 细胞中 WWC1、YAP、TAZ 和 CYR61 的蛋白表达。最后，取出异种移植瘤并检查肿瘤体积和重量。免疫组织化学染色和 Western blot 检测 NSCLC 的细胞增殖和凋亡。在这项研究中，结果表明 ACTL6A 在四种 NSCLC 细胞系中的 mRNA 和蛋白表达水平均高于正常肺细胞系。抑制 ACTL6A 抑制了 NSCLC 细胞的生长并促进了其凋亡。同时，ACTL6A 通过 Hippo/YAP 信号通路促进 NSCLC 肿瘤的生长并抑制其凋亡。ACTL6A 通过调节 Hippo/YAP 通路促进 NSCLC 中的增殖。
