Abstract
Reportedly, long‑chain non‑coding RNA LINC00963 features prominently in cancer biology. However, functional details of LINC00963 in colorectal cancer (CRC) remain to be elucidated. Reverse transcription‑quantitative (RT‑q)PCR was performed to examine LINC00963 and microRNA (miR)‑1281 expression levels in 53 matched pairs of cancerous and non‑cancerous tissues from patients with CRC. Tripartite motif‑containing 65 (TRIM65) protein expression in CRC cells was detected via western blot analysis. Furthermore, LINC00963 overexpression plasmid, LINC00963 small interfering RNA, miR‑1281 mimics or miR‑1281 inhibitors were transfected into CRC cells, and Cell Counting Kit‑8, colony formation and Transwell assays were adopted to study the effects of LINC00963 and miR‑1281 on the malignant phenotypes of CRC cells. Bioinformatics analysis, dual‑luciferase, RNA pull‑down and immunoprecipitation assays, RT‑qPCR and western blot analysis were performed to investigate the regulatory relationship between LINC00963, miR‑1281 and TRIM65. LINC00963 was highly expressed in CRC tissues and cells, while miR‑1281 was downregulated. Functionally, LINC00963 facilitated the proliferation, colony formation, migration and invasion of CRC cells, and increased the expression levels of Ki67, matrix metalloproteinase (MMP)2 and MMP9, while miR‑1281 had the opposite biological functions. Mechanistically, LINC00963 sponged miR‑1281 and repressed its expression in CRC cells, resulting in the upregulation of TRIM65. LINC00963 positively regulates TRIM65 in CRC progression by repressing miR‑1281 expression, showing potential as a therapeutic target for treating CRC.