A percentage of colorectal cancer (CRC) patients display low sensitivity to radiotherapy, which affects its therapeutic effect. Cancer cells DNA double-strand breaks (DSBs) repair capacity is crucial for radiosensitivity, but the roles of long noncoding RNAs (lncRNAs) in this process are largely uncharacterized. This study aims to explore whether lnc-RI regulates CRC cell growth and radiosensitivity by regulating the nonhomologous end-joining (NHEJ) repair pathway. CRC cells in which lnc-RI has been silenced showed lower cell growth and higher apoptosis rates due to increased DSBs and cell cycle arrest. We found that miR-4727-5p targets both lnc-RI and LIG4 mRNA and inhibit their expression. CRC cells showed increased radiosensitivity when lnc-RI was silenced. These results reveal novel roles for lnc-RI in both DNA damage repair and radiosensitivity regulation in CRC cells. Our study revealed that lnc-RI regulates LIG4 expression through lnc-RI/miR-4727-5p/LIG4 axis and regulates NHEJ repair efficiency to participate in DNA damage repair. The level of lnc-RI was negatively correlated with the radiosensitivity of CRC cells, indicates that lnc-RI may be a potential target for CRC therapy. We also present the first report of the function of miR-4727-5p.

一部分结直肠癌 (CRC) 患者对放疗的敏感性较低，这会影响其治疗效果。癌细胞 DNA 双链断裂 (DSBs) 修复能力对放射敏感性至关重要，但长链非编码 RNA (lncRNAs) 在此过程中的作用在很大程度上是未知的。本研究旨在探讨lnc-RI是否通过调节非同源末端连接 (NHEJ) 修复途径来调节 CRC 细胞生长和放射敏感性。由于 DSB 增加和细胞周期停滞，lnc-RI被沉默的CRC 细胞显示出较低的细胞生长和较高的细胞凋亡率。我们发现 miR-4727-5p 同时靶向 lnc -RI和LIG4mRNA 并抑制其表达。当lnc-RI沉默时，CRC 细胞显示出增加的放射敏感性。这些结果揭示了lnc-RI在 CRC 细胞的 DNA 损伤修复和放射敏感性调节中的新作用。我们的研究表明，lnc-R I通过lnc -RI /miR-4727-5p/ LIG4轴调节LIG4表达并调节NHEJ 修复效率参与DNA 损伤修复。lnc-RI水平与CRC细胞的放射敏感性呈负相关，表明lnc-RI可能是CRC治疗的潜在靶点。我们还首次报告了 miR-4727-5p 的功能。