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Decreased lncRNA TINCR promotes growth of colorectal carcinoma through upregulating microRNA-31

机译:降低LNCRNATINCR通过上调MicroRNA-31促进结肠直肠癌的生长

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摘要

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.
机译:在不同的人类癌症中报道了末端分化诱导的非分子RNA(TINCR),长期非编码RNA(LNCRNA)的异常表达,包括结肠直肠癌(CRC)。此外,利于CRC对CRC的效果的分子机制仍不清楚。这里,通过一组生物信息学研究,我们发现MicroRNA-31(miR-31)(miR-31),致力于CRC中鲁棒地上调的致癌miRNA是锡锡的海绵miRNA。在CRC组织和CRC细胞系中,TINCR和MIR-31水平呈逆转。荧光素酶报告器测定显示MIR-31的TINCR上的特异性结合位点。抑制TinCR在体外促进CRC细胞生长和迁移,而锡克的过度表达抑制了CRC细胞生长和体外迁移。 TINCR耗竭增加了体内肿瘤异种移植生长,而TINCR过表达抑制它。我们的研究表明,重新表达Tincr可以通过miR-31抑制CRC的侵入性。

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