Experimental analysis demonstrates that silencing Linc00284 enhances radiosensitivity in colorectal cancer, implicating miR-559 and c-Myc in the process.
Colorectal cancer (CRC), the most prevalent malignancy of the gastrointestinal tract, is commonly treated with radiotherapy; however, radioresistance often leads to poor prognosis. Long intergenic noncoding RNAs (LincRNAs), a subclass of long noncoding RNAs (lncRNAs), have been implicated in the pathogenesis of various cancers, including CRC, as well as in modulating radiosensitivity. In this study, qPCR analysis revealed that Linc00284 expression was significantly upregulated in CRC cells following radiotherapy, and its expression level was correlated with patient radiosensitivity. Furthermore, cell proliferation assays, colony formation assays, flow cytometry, and xenograft experiments confirmed that Linc00284 expression was notably upregulated in CRC cells post‐radiotherapy, and silencing Linc00284 significantly enhanced CRC radiosensitivity. Dual‐luciferase reporter assays demonstrated that Linc00284 directly bound to hsa‐miR‐559 (miR‐559) and negatively regulated its expression, ultimately upregulating MYC expression and promoting CRC cell proliferation. In conclusion, our findings highlighted the crucial role of Linc00284 in regulating the miR‐559/c‐Myc axis, which was pivotal for CRC radiosensitivity, and may provide valuable therapeutic targets for the management of CRC.
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Dong et al. (2025) studied this question.
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