MUC16在卵巢癌肿瘤生物学和肿瘤免疫学中的作用。

The role of MUC16 in tumor biology and tumor immunology in ovarian cancer.

作者信息

Yang Na, Zhou Xi, Gong Yangmei, Deng Zhizhi

机构信息

The First Affiliated Hospital, Gynecology & Obstetrics and Reproductive Medical Center, Hengyang Medical School, University of South China, No. 69, Chuanshan Avenue, Shigu District, Hengyang, 421001, Hunan Province, China.

出版信息

BMC Cancer. 2025 Feb 19;25(1):294. doi: 10.1186/s12885-025-13461-0.

DOI:10.1186/s12885-025-13461-0

PMID:39972413

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11837316/

Abstract

In this study, the influence of glycoproteomic changes, specifically MUC16, on NK cell-mediated immunotherapy response in ovarian cancer is explored. Analysis of glycoprotein data from the CPTAC database identified significant upregulation of MUC16 in ovarian cancer tissues, associated with tumor invasiveness and immune evasion. Experimental findings showed that MUC16 knockdown increased NK cell cytotoxicity, decreased invasiveness, and boosted NK cell activation, while MUC16 overexpression resulted in the opposite effects. In vivo experiments demonstrated that MUC16 knockdown suppressed tumor growth, enhanced NK cell infiltration, and bolstered NK cell activation, underscoring the potential of MUC16 as a target for novel immunotherapy approaches in ovarian cancer treatment.

摘要

在本研究中，探讨了糖蛋白质组学变化，特别是MUC16，对卵巢癌中自然杀伤（NK）细胞介导的免疫治疗反应的影响。对来自临床蛋白质组肿瘤分析联盟（CPTAC）数据库的糖蛋白数据进行分析，发现卵巢癌组织中MUC16显著上调，这与肿瘤侵袭性和免疫逃逸有关。实验结果表明，敲低MUC16可增加NK细胞的细胞毒性，降低侵袭性，并增强NK细胞的活化，而MUC16过表达则产生相反的效果。体内实验表明，敲低MUC16可抑制肿瘤生长，增强NK细胞浸润，并促进NK细胞活化，这突出了MUC16作为卵巢癌治疗新免疫治疗方法靶点的潜力。