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跨膜蛋白106A(TMEM106A)抑制肺癌细胞的增殖、迁移并诱导其凋亡。

TMEM106A inhibits cell proliferation, migration, and induces apoptosis of lung cancer cells.

作者信息

Liu Juncai, Zhu Hongjing

机构信息

Department of Radiotherapy, Huaihe Hospital, Henan University, Kaifeng, China.

Department of Nuclear Medicine, Huaihe Hospital, Henan University, Kaifeng, China.

出版信息

J Cell Biochem. 2019 May;120(5):7825-7833. doi: 10.1002/jcb.28057. Epub 2018 Nov 19.

DOI:10.1002/jcb.28057
PMID:30456879
Abstract

Transmembrane protein 106A (TMEM106A) has been found to function as tumor suppressor in gastric and renal cancer. However, the role of TMEM106A in nonsmall-cell lung carcinoma (NSCLC) has not been investigated. In this study, we evaluated the expression profile of TMEM106A in NSCLC tissues and cell line, and explored the roles of TMEM106A in NSCLC cell lines. Our results showed that TMEM106A expression was significantly decreased in human NSCLC tissues. In vitro assays showed that TMEM106A expression in NSCLC cell lines was much lower than that in the bronchial epithelial cell line. Besides, overexpression of TMEM106A reduced cell proliferation, migration, and invasion, while induced cell apoptosis in NSCLC cells. TMEM106A overexpression repressed epithelial-mesenchymal transition (EMT), which was illustrated by increased E-cadherin expression and decreased the expressions of N-cadherin, and vimentin. In addition, TMEM106A overexpression suppressed the activation of phosphoinositide 3-kinase/protein kinase B/nuclear factor-κB (PI3K/Akt/NF-κB) signaling pathway in NSCLC cells. Our results indicated that TMEM106A acted as a tumor suppressor in NSCLC, and could be a therapeutic target for the management of NSCLC.

摘要

跨膜蛋白106A(TMEM106A)已被发现可作为胃癌和肾癌的肿瘤抑制因子。然而,TMEM106A在非小细胞肺癌(NSCLC)中的作用尚未得到研究。在本研究中,我们评估了TMEM106A在NSCLC组织和细胞系中的表达谱,并探讨了TMEM106A在NSCLC细胞系中的作用。我们的结果表明,TMEM106A在人类NSCLC组织中的表达显著降低。体外实验表明,NSCLC细胞系中TMEM106A的表达远低于支气管上皮细胞系。此外,TMEM106A的过表达降低了NSCLC细胞的增殖、迁移和侵袭能力,同时诱导了细胞凋亡。TMEM106A的过表达抑制了上皮-间质转化(EMT),这表现为E-钙黏蛋白表达增加,N-钙黏蛋白和波形蛋白表达降低。此外,TMEM106A的过表达抑制了NSCLC细胞中磷酸肌醇3-激酶/蛋白激酶B/核因子-κB(PI3K/Akt/NF-κB)信号通路的激活。我们的结果表明,TMEM106A在NSCLC中起肿瘤抑制作用,可能是NSCLC治疗的一个靶点。

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