FHL1过表达通过增加RhoGDIß mRNA表达抑制肺癌细胞侵袭

Yanbo Zhang, Xuefeng Wang, Peng Wang, Xingle Zhang, Shangzhi Han, F. Huo
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引用次数: 2

摘要

目的许多lncrna与口腔鳞状细胞癌(OSCC)的进展有关。本研究旨在探讨lncRNA DS细胞粘附分子反义RNA 1 (DSCAM-AS1)在OSCC中的功能作用及分子机制。材料与方法在本实验研究中,共收集术中OSCC标本及癌旁组织46对。在OSCC组织和细胞系中,采用定量实时聚合酶链反应(qRT- PCR)检测DSCAM-AS1和microRNA-138-5p (miR-138-5p)的表达水平。Western blot检测zeste 2 polycomb suppression complex 2亚单位(EZH2)增强子表达水平。然后,在OSCC细胞中用siRNA敲低DSCAM-AS1,并进行MTT和EdU试验来评估OSCC细胞的增殖情况。Transwell法检测OSCC细胞迁移和侵袭能力。此外,通过RNA免疫沉淀、双荧光素酶报告基因检测、qRT-PCR、Western blot等方法探讨DSCAM-AS1、miR-138-5p、EZH2之间的关系。结果DSCAM-AS1在OSCC组织和细胞系中的表达显著升高,敲低DSCAM-AS1可显著抑制OSCC细胞的增殖、迁移和侵袭。MiR-138-5p被确定为DSCAM-AS1的靶标,其抑制剂可以逆转DSCAM-AS1敲低对OSCC进展的抑制作用。EZH2被证实是miR-138-5p的靶标,EZH2敲低可以抵消miR-138-5p抑制剂对OSCC进展的促进作用。此外,DSCAM-AS1作为ceRNA可通过miR-138-5p调控EZH2的表达。结论DSCAM-AS1可通过miR-138-5p/EZH2轴在OSCC中发挥促瘤作用。
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FHL1 Overexpression as A Inhibitor of Lung Cancer Cell Invasion via Increasing RhoGDIß mRNA Expression
Objective A lot of lncRNAs are implicated in oral squamous cell carcinoma (OSCC) progression. The study aimed at investigating lncRNA DS cell adhesion molecule antisense RNA 1 (DSCAM-AS1)’s functional role and molecular mechanism in OSCC. Materials and Methods In this experimental study, a total of 46 pairs of OSCC samples and para-cancerous tissues were collected during surgery. In OSCC tissues and cell lines, quantitative real time polymerase chain reaction (qRT- PCR) was performed for detecting DSCAM-AS1 and microRNA-138-5p (miR-138-5p) expression levels. Western blot was conducted to examine the enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) expression level. Then, DSCAM-AS1 was knocked down with siRNA in OSCC cells and MTT and EdU assays were conducted to evaluate OSCC cell proliferation. Transwell assay was utilized for detecting OSCC cell migration and invasion capacities. Besides, the relationships among DSCAM-AS1, miR-138-5p, and EZH2 were explored through RNA immunoprecipitation, dual-luciferase reporter assay, qRT-PCR, and Western blot. Results DSCAM-AS1 expression was remarkably increased in OSCC tissues and cell lines, and DSCAM-AS1 knockdown could significantly restrain OSCC cell proliferation, migration, and invasion. MiR-138-5p was identified as a target of DSCAM-AS1, and its inhibitor could reverse the suppressive effects of DSCAM-AS1 knockdown on OSCC progression. EZH2 was verified as a target of miR-138-5p, and EZH2 knockdown could counteract the promotional impact of miR-138-5p inhibitor on OSCC progression. Additionally, DSCAM-AS1, as a ceRNA, could regulate EZH2 expression via miR-138-5p. Conclusion DSCAM-AS1 can play a tumor-promoting role in OSCC via miR-138-5p/EZH2 axis.
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