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.
Keywords: colorectal carcinoma (CRC); long non-coding RNA (lncRNA); microRNA-31 (miR-31); terminal differentiation-induced noncoding RNA (TINCR).