Endoscopy Center, Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Aging (Albany NY). 2020 Jul 17;12(14):14219-14231. doi: 10.18632/aging.103436.
Abnormal expression in terminal differentiation-induced noncoding RNA (TINCR), a long non-coding RNA (lncRNA), has been reported in different human cancers, including colorectal carcinoma (CRC). Moreover, the molecular mechanisms that underlie the effects of TINCR on CRC remain unclear. Here, by a set of bioinformatics studies, we found that microRNA-31 (miR-31), the oncogenic miRNA that robustly upregulates in CRC, was a sponge miRNA for TINCR. TINCR and miR-31 levels were inversely correlated in both CRC tissues and CRC cell lines. Luciferase reporter assay revealed a specific binding site on TINCR for miR-31. Suppression of TINCR promoted CRC cell growth and migration in vitro, while overexpression of TINCR inhibited CRC cell growth and migration in vitro. TINCR depletion increased tumor xenograft growth in vivo, while TINCR overexpression inhibited it. Together, our study suggests that re-expressing TINCR may suppress invasive outgrowth of CRC through miR-31.
终端分化诱导非编码 RNA(TINCR)是一种长非编码 RNA(lncRNA),其异常表达已在多种人类癌症中报道,包括结直肠癌(CRC)。此外,TINCR 对 CRC 影响的分子机制尚不清楚。在这里,通过一系列的生物信息学研究,我们发现 microRNA-31(miR-31),即 CRC 中强烈上调的致癌 miRNA,是 TINCR 的海绵 miRNA。CRC 组织和 CRC 细胞系中 TINCR 和 miR-31 的水平呈负相关。荧光素酶报告基因检测显示 TINCR 上存在 miR-31 的特异性结合位点。抑制 TINCR 促进 CRC 细胞的体外生长和迁移,而过表达 TINCR 则抑制 CRC 细胞的体外生长和迁移。TINCR 耗竭增加体内肿瘤异种移植物的生长,而过表达 TINCR 则抑制其生长。综上所述,我们的研究表明,重新表达 TINCR 可能通过 miR-31 抑制 CRC 的侵袭性生长。