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从防御到疾病:免疫系统如何助力卵巢癌中的上皮-间质转化

From Defense to Disease: How the Immune System Fuels Epithelial-Mesenchymal Transition in Ovarian Cancer.

作者信息

Kos Michał, Mertowska Paulina, Mertowski Sebastian, Roliński Jacek, Krasińska-Płachta Aleksandra, Urbanowicz Tomasz, Gogacz Marek, Grywalska Ewelina

机构信息

II Clinic of Gynecology, Medical University of Lublin, 20-093 Lublin, Poland.

Department of Experimental Immunology, Medical University of Lublin, 20-093 Lublin, Poland.

出版信息

Int J Mol Sci. 2025 Apr 24;26(9):4041. doi: 10.3390/ijms26094041.

DOI:10.3390/ijms26094041
PMID:40362280
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12072087/
Abstract

Ovarian cancer is one of the most deadly gynecological cancers, with over 300 thousand new cases per year, most of which are diagnosed in advanced stages. The limited availability of effective biomarkers and lack of characteristic symptoms make early diagnosis difficult, resulting in a five-year survival rate of 30-40%. Mutations in the and genes and abnormalities of signaling pathways such as PI3K/AKT and TP53 play a key role in the progression of ovarian cancer. The immune system, which can act against tumors, often supports tumor development in the ovarian cancer microenvironment through immunoevasion, which is influenced by cytokines such as IL-6, IL-10, and TGF-β. Epithelial-to-mesenchymal transition (EMT) allows cancer cells to acquire mesenchymal characteristics, increasing their invasiveness and metastatic capacity. Immunological factors, including pro-inflammatory cytokines and signals from the tumor microenvironment regulate the EMT process. This review aims to present the role of EMT in ovarian cancer progression, its interactions with the immune system, and potential biomarkers and therapeutic targets. Modulation of the immune response and inhibition of EMT may constitute the basis for personalized therapies, which opens new possibilities for improving the prognosis and efficacy of treatment in patients with ovarian cancer.

摘要

卵巢癌是最致命的妇科癌症之一,每年有超过30万新发病例,其中大多数在晚期被诊断出来。有效生物标志物的可用性有限以及缺乏特征性症状使得早期诊断困难,导致五年生存率为30-40%。BRCA1和BRCA2基因的突变以及PI3K/AKT和TP53等信号通路的异常在卵巢癌进展中起关键作用。免疫系统本可对抗肿瘤,但在卵巢癌微环境中,它常通过免疫逃逸支持肿瘤发展,而免疫逃逸受IL-6、IL-10和TGF-β等细胞因子影响。上皮-间质转化(EMT)使癌细胞获得间质特征,增加其侵袭性和转移能力。免疫因素,包括促炎细胞因子和肿瘤微环境的信号调节EMT过程。本综述旨在阐述EMT在卵巢癌进展中的作用、其与免疫系统的相互作用以及潜在的生物标志物和治疗靶点。调节免疫反应和抑制EMT可能构成个性化治疗的基础,这为改善卵巢癌患者的预后和治疗效果开辟了新的可能性。

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