Long non-coding RNA LINC00707 acts as a competing endogenous RNA to enhance cell proliferation in colorectal cancer.

Long non-coding RNAs (lncRNAs) have been indicated to serve critical roles in cancer development and progression. Long intergenic non-protein coding RNA 70 (LINC00707) was recently reported to be an oncogene involved in the tumorigenesis of several types of human cancer. However, the clinical role, biological functions and molecular mechanism of LINC00707 in colorectal cancer (CRC) remain unclear. The aim of the present study was to investigate the biological effects and mechanism of LINC00707 in CRC. Reverse transcription-quantitative PCR was used to detect the expression levels of LINC00707 in 65 CRC tissue samples and CRC cell lines (HCT116, HT29 and SW480). Cell Counting Kit-8 and colony formation assays were performed to investigate the effects of LINC00707 on CRC cell proliferation. A dual-luciferase reporter assay was conducted to investigate the mechanisms of LINC00707 in CRC. The upregulation of LINC00707 expression was significantly associated with tumor size, stage and poor survival in patients with CRC. LINC00707 also acted as an independent prognostic factor for CRC. Functional analyses revealed that the knockdown of LINC00707 could inhibit CRC cell proliferation. Furthermore, bioinformatics analysis demonstrated that microRNA (miR)-485-5p could directly bind to LINC00707, which was confirmed by a dual-luciferase reporter assay. In conclusion, the upregulation of LINC00707 is associated with a shorter survival time in patients with CRC. Knockdown of LINC00707 may inhibit the proliferation of CRC cells by binding with miR-485-5p.