KCTD10促进PD-L1在结直肠癌中的表达,增强了PD-1抗体的抗肿瘤作用。

IF 1.4
Zihao Yin, Rongyu Su, Shengwen Long, Guo Chen, Shuanglin Xiang
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引用次数: 0

摘要

结直肠癌是一种非常普遍的消化道恶性肿瘤。免疫治疗已成为结直肠癌患者的一种重要治疗方法。我们观察到,与正常组织相比,KCTD10在结直肠癌组织中的表达显著下调,KCTD10表达较高的患者存活时间更长。为了研究其功能作用,我们建立了稳定的过表达kctd10的CT26和SW480结直肠癌细胞系。体外和体内实验均表明,KCTD10过表达可抑制结直肠癌的进展并抑制EMT过程。值得注意的是,KCTD10过表达上调PD-L1表达,协同增强抗pd -1治疗的疗效。我们的研究结果表明,KCTD10在结直肠癌的发病机制中起肿瘤抑制作用。在机制上,KCTD10通过上调PD-L1表达来增强抗pd -1免疫治疗的抗肿瘤效果,从而提出了一种新的治疗靶点,并为CRC治疗提供了一种有希望的联合策略。KCTD10可以抑制结直肠癌的发展和EMT过程。而过表达KCTD10可增加PD-L1的表达,提高PD-1治疗的疗效。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
KCTD10 promoting PD-L1 expression in colorectal cancer enhanced the anti-tumor effect of PD-1 antibody.

Colorectal cancer is a highly prevalent malignant tumor of the digestive tract worldwide. Immunotherapy has emerged as a critical therapeutic approach for CRC patients. We observed that KCTD10 expression is significantly downregulated in colorectal cancer tissues compared to normal tissues, and patients with higher KCTD10 expression exhibited prolonged survival. To investigate its functional role, we established stable KCTD10-overexpressing CT26 and SW480 colorectal cancer cell lines. Both in vitro and in vivo experiments demonstrated that KCTD10 overexpression suppresses colorectal cancer progression and inhibits the EMT process. Notably, KCTD10 overexpression upregulated PD-L1 expression and synergistically enhanced the therapeutic efficacy of anti-PD-1 treatment. Our findings reveal that KCTD10 functions as a tumor suppressor in colorectal cancer pathogenesis. Mechanistically, KCTD10 potentiates the antitumor efficacy of anti-PD-1 immunotherapy by upregulating PD-L1 expression, thereby proposing a novel therapeutic target and suggesting a promising combination strategy for CRC treatment. Insight box KCTD10 can inhibit the development of colorectal cancer and the EMT process. And the over-expression of KCTD10 increased the expression of PD-L1, improved the efficacy of PD-1 treatment.

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