Department of Gynaecology, University of Chinese Academy of Sciences Shenzhen Hospital, No. 4253 Songbai Road, Matian Street, Guangming District, Shenzhen City, 518106, Guangdong Province, China.
Department of Gynaecology, Affiliated Hospital of Chengde Medical University, Chengde, 067000, Hebei, China.
Hum Cell. 2019 Oct;32(4):515-521. doi: 10.1007/s13577-019-00268-y. Epub 2019 Aug 6.
This study aimed to investigate the role of lncRNA terminal differentiation-induced ncRNA (TINCR) in cervical squamous cell carcinoma (CSCC). By informatics analysis, we found that miR-302 may bind TINCR. Expression analysis showed that miR-302 was downregulated, while TINCR was upregulated in CSCC. Correlation analysis showed that they were not significantly correlated. In CSCC cells, miR-302 and TINCR failed to affect the expression of each other. However, miR-302 overexpression led to downregulated and TINCR overexpression led to upregulated cyclin D1 expression in CSCC cells. Interestingly, overexpression of cyclin D1 led to upregulated miR-302 and TINCR. Cell proliferation analysis showed that TINCR and cyclin D1 overexpression led to increased, while miR-302 overexpression led to decreased rate of cell proliferation. Moreover, miR-302 overexpression reduced the effects of TINCR overexpression. Therefore, TINCR sponges miR-302 to upregulate cyclin D1 in CSCC, thereby promoting cell proliferation.
本研究旨在探讨长链非编码 RNA 终端分化诱导的非编码 RNA(TINCR)在宫颈鳞状细胞癌(CSCC)中的作用。通过信息学分析,我们发现 miR-302 可能与 TINCR 结合。表达分析显示,miR-302 在 CSCC 中下调,而 TINCR 上调。相关性分析表明它们之间没有显著相关性。在 CSCC 细胞中,miR-302 和 TINCR 不能相互影响彼此的表达。然而,miR-302 的过表达导致 CSCC 细胞中环蛋白 D1 的表达下调,而 TINCR 的过表达导致环蛋白 D1 的表达上调。有趣的是,cyclin D1 的过表达导致 miR-302 和 TINCR 的上调。细胞增殖分析表明,TINCR 和 cyclin D1 的过表达导致细胞增殖率增加,而 miR-302 的过表达导致细胞增殖率降低。此外,miR-302 的过表达降低了 TINCR 过表达的影响。因此,TINCR 海绵 miR-302 上调 CSCC 中的 cyclin D1,从而促进细胞增殖。