Upregulation of Linc00960 promotes colorectal cancer cell proliferation by regulating hsa-miR-107/CDK6 axis

Colorectal cancer (CRC), the most common gastrointestinal malignancy, has incompletely understood underlying developmental mechanisms. LincRNA, a subclass of long non-coding RNAs (LncRNAs), is implicated in the pathogenesis of multiple cancers, including CRC. In this study, qPCR analysis revealed that Linc00960 expression was significantly upregulated in CRC tissues compared to adjacent non-tumor tissues and correlated with poor patient prognosis. Functional assays (including cell proliferation, colony formation, flow cytometry, Transwell assay and xenograft experiments) demonstrated that high Linc00960 expression enhanced CRC cell proliferation, whereas Linc00960 knockdown markedly suppressed cell proliferation, migration and invasion. To investigate the mechanism, dual-luciferase reporter assays were performed; there revealed that Linc00960 directly bound to hsa-miR-107 (miR-107) and negatively regulated its expression, thereby upregulating CDK6 expression and promoting CRC cell proliferation. In conclusion, our findings indicated that the Linc00960/miR-107/CDK6 axis served as a crucial signaling pathway in CRC progression, providing novel potential targets and biomarkers for CRC diagnosis and therapy.