本研究的目的是探讨DGUOK在结直肠癌（CRC）进展中的作用及其对CRC细胞对5-FU治疗敏感性的影响。我们进行了生物信息学分析和qRT-PCR来评估DGUOK表达在结直肠癌组织/细胞中。使用 CCK-8 和集落形成测定评估用 5-FU 处理的 CRC 细胞的细胞活力。通过免疫荧光测定和蛋白质印迹分析测定自噬水平。此外，通过蛋白质印迹研究了 p-p38 对自噬的影响。我们进行了救援实验，以确认 DGUOK/p38 是否通过自噬影响 CRC 细胞中的 5-FU 敏感性。我们的研究结果表明，与正常组织相比，DGUOK 在 CRC 组织中表达上调，与细胞增殖和迁移增加相关。从功能上讲，抑制 DGUOK 会增强自噬，从而降低 CRC 细胞对 5-FU 的敏感性。这种效应部分是由 DGUOK 对丝裂原激活蛋白激酶 (MAPK) 途径的影响介导的，特别是促进 p38 MAPK 的磷酸化，p38 MAPK 是自噬途径的关键调节因子。这些结果表明 DGUOK 可以作为一种新的标记物用于预测 5-FU 在 CRC 治疗中的功效。版权所有© Bentham Science Publishers；如有任何疑问，请发送电子邮件至 epub@benthamscience.net。

The purpose of this study was to investigate the role of DGUOK in the pro-gression of colorectal cancer (CRC) and its impact on the sensitivity of CRC cells to 5-FU treatment.We conducted bioinformatics analysis and qRT-PCR to evaluate DGUOK expression in CRC tissues/cells. Cell viability of CRC cells treated with 5-FU was assessed using CCK-8 and colony formation assays. Autophagy levels were determined through immunofluorescence assays and Western blot analysis. Additionally, the influence of p-p38 on autophagy was inves-tigated via Western blotting. A rescue assay was performed to confirm whether DGUOK/p38 affects 5-FU sensitivity in CRC cells through autophagy.Our findings indicate that DGUOK is upregulated in CRC tissues compared to normal tissues, correlating with increased cell proliferation and migration. Functionally, inhibition of DGUOK enhances autophagy, thereby decreasing the sensitivity of CRC cells to 5-FU. This ef-fect is partly mediated by DGUOK's impact on the mitogen-activated protein kinase (MAPK) pathway, specifically promoting the phosphorylation of p38 MAPK, a crucial regulator in au-tophagy pathways.These results suggest that DGUOK could serve as a novel marker for predicting the efficacy of 5-FU in CRC treatment.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.