Long non-coding RNA OTUD6B-AS1 overexpression inhibits the proliferation, invasion and migration of colorectal cancer cells via downregulation of microRNA-3171.

Colorectal cancer (CRC) is a common digestive system malignancy and a major cause of cancer-associated mortality worldwide. Aberrant expression of long non-coding RNAs has been reported in several types of cancer. The aim of the present study was to investigate the role of ovarian tumor domain containing 6B antisense RNA1 (OTUD6B-AS1) in CRC and its underlying mechanisms. OTUD6B-AS1 expression in CRC cell lines was examined using reverse transcription-quantitative PCR. Furthermore, The Cancer Genome Atlas database was utilized to examine the expression levels of OTUD6B-AS1 in CRC tissues. Following OTUD6B-AS1 overexpression, Cell Counting Kit-8 and colony formation assays were used to detect the proliferation ability of HCT116 cells. The expression levels of proliferation-related protein Ki67 were determined using immunofluorescence staining. Subsequently, Transwell and wound healing assays were used to evaluate the invasion and migration of HCT116 cells, respectively. The expression levels of migration-related proteins (MMP2 and MMP9) were measured using western blotting. Additionally, a luciferase reporter assay was used to verify the potential interaction between OTUD6B-AS1 and microRNA-3171 (miR-3171). Subsequently, rescue assays were performed to clarify the regulatory effects of OTUD6B-AS1 and miR-3171 on CRC development. The results demonstrated that OTUD6B-AS1 expression was low in CRC cells and tissues. Overexpression of OTUD6B-AS1 inhibited the proliferation, invasion and migration of HCT116 cells. Furthermore, miR-3171 was demonstrated to be a direct target of OTUD6B-AS1 using a luciferase reporter assay. The rescue assays revealed that miR-3171 mimics markedly reversed the inhibitory effects of OTUD6B-AS1 overexpression on proliferation, invasion and migration of CRC cells. Overall, these findings demonstrated that OTUD6B-AS1 overexpression inhibited the proliferation, invasion and migration of HCT116 cells via downregulation of miR-3171, suggesting that OTUD6B-AS1 may serve as a novel biomarker for CRC treatment.