Guo Yan, Ren Mei-Si, Shang Chao, Zhu Li, Zhong Ming
Key Laboratory of Liaoning Province Oral Disease, School of Stomatology, China Medical University Shenyang 110002, P. R. China.
Department of Pathology, School of Stomatology, China Medical University Shenyang 110002, P. R. China.
Int J Clin Exp Med. 2015 Sep 15;8(9):15441-9. eCollection 2015.
Metastasis suppressor-1 (MTSS1) is a novel potential metastasis suppressor gene in several types of human cancers. However, the exact function and regulatory mechanism of MTSS1 in Tongue squamous cellular carcinoma (TSCC) have not been elucidated.
MATERIAL/METHODS: We first confirmed the MTSS1 gene expression by using quantitative real time-PCR (qRT-PCR) and immunohistochemical staining. Then we detected the effect of MTSS1 gene on Tca8113 cells proliferation and invasion ability by using MTT, wound healing and invasion assay. Finally by using bioinformatics analysis, luciferase reporter assay and a serial method, we analyzed the targeting of miR-96 on MTSS1 and the ability of miR-96 on MTSS1 gene mediated biological alterations in Tca8113 cells.
Our findings showed that the expression of MTSS1 was down-regulated in both TSCC tissues and Tca8113 cells. Forced expression of MTSS1 led to inhibited cell proliferation ability, retarded wound closing and reduced trans-membrane cell numbers. MiR-96 is confirmed to be a direct target of MTSS1 gene and could regulate MTSS1 mediated Tca8113 cells proliferation and metastasis. But miR-96 could not completely restore the invasion ability of Tca8113 cells.
MiR-96 targeting and promoting MTSS1 repression may precipitate in the TSCC tumorigenesis through bypassing cell proliferation and metastasis control.
转移抑制因子1（MTSS1）是多种人类癌症中一种新的潜在转移抑制基因。然而，MTSS1在舌鳞状细胞癌（TSCC）中的确切功能和调控机制尚未阐明。
材料/方法：我们首先通过定量实时聚合酶链反应（qRT-PCR）和免疫组织化学染色来确认MTSS1基因的表达。然后我们通过MTT、伤口愈合和侵袭实验检测MTSS1基因对Tca8113细胞增殖和侵袭能力的影响。最后，通过生物信息学分析、荧光素酶报告基因检测和一系列方法，我们分析了miR-96对MTSS1的靶向作用以及miR-96对MTSS1基因介导的Tca8113细胞生物学改变的影响。
我们的研究结果表明，MTSS1在TSCC组织和Tca8113细胞中的表达均下调。MTSS1的强制表达导致细胞增殖能力受到抑制、伤口愈合延迟和跨膜细胞数量减少。miR-96被证实是MTSS1基因的直接靶点，并且可以调节MTSS1介导的Tca8113细胞增殖和转移。但是miR-96不能完全恢复Tca8113细胞的侵袭能力。
miR-96靶向并促进MTSS1的抑制可能通过绕过细胞增殖和转移控制而促使TSCC的肿瘤发生。
