Noncoding RNA Linc00475 promotes the proliferation of colorectal cancer cells by targeting miR‐107/CDK6 axis

Colorectal cancer (CRC) represents a substantial challenge to public health. Despite extensive research, the pathogenesis of CRC is not yet fully elucidated, hindering the development of effective therapeutic strategies. Recent advancements have underscored the importance of Non‐coding RNAs in tumor biology. Our research identified a significant upregulation of Linc00475 in CRC, which correlated with reduced survival rates among CRC patients. Consequently, this study aimed to elucidate the mechanisms by which Linc00475 contributed to CRC progression. Employing a comprehensive array of experimental techniques—including CCK‐8 assays, colony formation assays, flow cytometry, quantitative PCR (qPCR), western blot analysis, and in vivo tumorigenesis assays—we have demonstrated that Linc00475 enhances CRC cell proliferation. Further analysis revealed that Linc00475 directly interacted with miR‐107, leading to its downregulation. Moreover, our findings confirmed that miR‐107 directly targeted CDK6, which was markedly downregulated following Linc00475 silencing. In vivo experiments further indicated that the silencing of Linc00475 markedly inhibited the proliferation of CRC cells. Collectively, our findings suggested that Linc00475 facilitated CRC cell proliferation through the regulation of the miR‐107/CDK6 axis, thereby providing a novel perspective for understanding the molecular mechanisms underlying CRC development. Noncoding RNA Linc00475 facilitated the proliferation of colorectal cancer (CRC) cells and was associated with poor survival outcomes by inhibiting miR‐107 and subsequently upregulating CDK6 expression. The Linc00475‐miR‐107‐CDK6 axis presents a promising therapeutic target for CRC.