LncRNA LINC00963 downregulation regulates colorectal cancer tumorigenesis and progression via the miR‑10b/FGF13 axis.

Abstract

Long non-coding RNAs (lncRNAs) serve a key role in different types of cancer, including colorectal cancer (CRC). The exact roles and mechanisms underlying lncRNA00963 [long intergenic non-protein coding RNA 963 (LINC00963)] in CRC are not completely understood. The present study aimed to identify the effects and mechanisms underlying LINC00963 in CRC. Firstly, the LINC00963 expression was detected using reverse transcription-quantitative PCR and the results demonstrated that LINC00963 expression levels were significantly increased in CRC tissues and cell lines compared with healthy tissues and HpoEpiC cells, respectively. Online database analysis indicated that high levels of LINC00963 were associated with low survival rates. The results of functional experiments, such as CCK-8 assay, colony formation assay, wound healing assay and Transwell invasion assay, indicated that LINC00963 knockdown significantly inhibited CRC cell proliferation, colony formation, migration and invasion compared with the small interfering RNA (si)-negative control (NC) group. Furthermore, the luciferase reporter indicated that LINC00963 competitively regulated microRNA (miR)-10b by targeting fibroblast growth factor 13 (FGF13). Compared with si-NC, LINC00963 knockdown decreased the expression levels of FGF13, vimentin and N-cadherin, and increased the expression of E-cadherin as detecting by western blotting. miR-10b inhibitors partly attenuated si-LINC00963-induced inhibition of CRC cell proliferation, migration and invasion. Collectively, the results of the present study suggested a potential role of the LINC00963/miR-10b/FGF13 axis in the tumorigenesis and progression of CRC, indicating a novel lncRNA-based diagnostic or therapeutic target for CRC.