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免疫反应性微环境调节剂GBP5通过诱导典型细胞焦亡抑制卵巢癌进展。

Immunoreactive Microenvironment Modulator GBP5 Suppresses Ovarian Cancer Progression by Inducing Canonical Pyroptosis.

作者信息

Zou Chang, Shen Jiacheng, Xu Fangfang, Ye Yingjun, Wu Yuanyuan, Xu Shaohua

机构信息

Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai 200092, China.

出版信息

J Cancer. 2024 May 5;15(11):3510-3530. doi: 10.7150/jca.94616. eCollection 2024.

DOI:10.7150/jca.94616
PMID:38817865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11134437/
Abstract

Ovarian cancer has the highest mortality among gynecological malignancies, and exploring effective strategies to reverse the immunosuppressive tumor microenvironment in patients remains a pressing scientific challenge. In this study, we identified a pyroptosis-related protective factor, GBP5, which significantly inhibits the growth of ovarian cancer cells and patient-derived ovarian cancer organoids, impeding the invasion and migration of ovarian cancer cells. Results of immunohistochemistry and external single-cell data verification were consistent. Further research confirmed that GBP5 in ovarian cancer cell can induce canonical pyroptosis through JAK2/STAT1 pathway, thereby restraining the progression of ovarian cancer. Interestingly, in this study, we also discovered that ovarian cancer cells with high GBP5 expression exhibit increased expressions of CXCL9/10/11 in a co-culture assay. Subsequent immune cell infiltration analyses revealed the remodeling of immunosuppressive microenvironment in ovarian cancer patients, characterized by increased infiltration and polarization of M1 macrophages. External immunotherapy database analysis showed profound potential for the application of GBP5 in immunotherapy strategies for ovarian cancer. Overall, our study demonstrates that the protective factor GBP5 significantly inhibits ovarian cancer progression, triggering canonical pyroptosis through the JAK2-STAT1 pathway. Driven by its pro-inflammatory nature, it can also enhance M1 macrophages polarization and reverse immunosuppressive microenvironment, thus providing new insights for ovarian cancer treatment.

摘要

卵巢癌在妇科恶性肿瘤中死亡率最高，探索有效的策略来逆转患者免疫抑制性肿瘤微环境仍然是一项紧迫的科学挑战。在本研究中，我们鉴定出一种与细胞焦亡相关的保护因子GBP5，它能显著抑制卵巢癌细胞和患者来源的卵巢癌类器官的生长，阻碍卵巢癌细胞的侵袭和迁移。免疫组化结果和外部单细胞数据验证结果一致。进一步研究证实，卵巢癌细胞中的GBP5可通过JAK2/STAT1途径诱导典型的细胞焦亡，从而抑制卵巢癌的进展。有趣的是，在本研究中，我们还发现，在共培养实验中，高表达GBP5的卵巢癌细胞CXCL9/10/11的表达增加。随后的免疫细胞浸润分析揭示了卵巢癌患者免疫抑制微环境的重塑，其特征是M1巨噬细胞浸润和极化增加。外部免疫治疗数据库分析显示GBP5在卵巢癌免疫治疗策略中的应用具有巨大潜力。总体而言，我们的研究表明，保护因子GBP5通过JAK2-STAT1途径显著抑制卵巢癌进展，引发典型的细胞焦亡。受其促炎性质驱动，它还可增强M1巨噬细胞极化并逆转免疫抑制微环境，从而为卵巢癌治疗提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c5f/11134437/e6fb8ed77747/jcav15p3510g010.jpg
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