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探索细胞死亡调控在妇科肿瘤免疫治疗中的潜在价值。

Exploring the Potential Value of Modulation of Cell Death in Immunotherapy of Gynecological Tumors.

作者信息

Wang Jiajun, Luo Ning, Wu Yuliang, Cheng Zhongping

机构信息

Department of Gynecology and Obstetrics, Tenth People's Hospital Affiliated to Tongji University, Shanghai, China.

出版信息

Gynecol Minim Invasive Ther. 2025 May 22;14(2):109-117. doi: 10.4103/gmit.GMIT-D-24-00005. eCollection 2025 Apr-Jun.

DOI:10.4103/gmit.GMIT-D-24-00005
PMID:40521585
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12165680/
Abstract

Cell death plays a pivotal role in a multitude of biological processes, including embryonic development, organ maintenance, aging, immune response, and autoimmunity. These processes are underpinned by distinct molecular mechanisms and have significant implications for biological systems. Currently, research on regulatory cell death (RCD) is primarily focused on apoptosis, necroptosis, pyroptosis, ferroptosis, cuproptosis, and autophagy. These pathways have been shown to play a crucial role in regulating the tumor microenvironment (TME) and influencing the clinical outcome of cancer immunotherapy. RCD exerts a dual regulatory effect on TME, releasing intracellular components and regulating the distribution of immune cells. These cells are involved in fine-tuning the antitumor immune response in the TME. The treatment of gynecological tumors frequently presents a challenge due to the lack of immunotherapeutic responsiveness. This review will focus on apoptosis, necroptosis, pyroptosis, ferroptosis, cuproptosis, and autophagy. It will explore how the molecular messengers released during these processes are involved in regulating their complex interactions with tumor tissues as well as with the immune response. It will also analyze the immunological consequences of regulated cell death and its potential impact on the future development of gynecological oncology therapy. By investigating the mechanisms of cell death, we can gain insight into their role in the development of gynecological tumors and potentially identify new therapeutic strategies to enhance the efficacy of existing treatments and advance cancer care.

摘要

细胞死亡在众多生物学过程中起着关键作用,包括胚胎发育、器官维持、衰老、免疫反应和自身免疫。这些过程由独特的分子机制支撑,对生物系统具有重要意义。目前,关于调节性细胞死亡(RCD)的研究主要集中在凋亡、坏死性凋亡、焦亡、铁死亡、铜死亡和自噬。这些途径已被证明在调节肿瘤微环境(TME)和影响癌症免疫治疗的临床结果中起关键作用。RCD对TME发挥双重调节作用,释放细胞内成分并调节免疫细胞的分布。这些细胞参与微调TME中的抗肿瘤免疫反应。由于缺乏免疫治疗反应性,妇科肿瘤的治疗常常面临挑战。本综述将聚焦于凋亡、坏死性凋亡、焦亡、铁死亡、铜死亡和自噬。它将探讨这些过程中释放的分子信使如何参与调节它们与肿瘤组织以及免疫反应的复杂相互作用。它还将分析调节性细胞死亡的免疫学后果及其对妇科肿瘤治疗未来发展的潜在影响。通过研究细胞死亡机制,我们可以深入了解它们在妇科肿瘤发生发展中的作用,并有可能确定新的治疗策略,以提高现有治疗的疗效并推进癌症护理。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5794/12165680/ec63aabbee68/GMIT-14-109-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5794/12165680/ec63aabbee68/GMIT-14-109-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5794/12165680/ec63aabbee68/GMIT-14-109-g001.jpg

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本文引用的文献

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VDX-111, a novel small molecule, induces necroptosis to inhibit ovarian cancer progression.新型小分子 VDX-111 通过诱导细胞坏死抑制卵巢癌进展。
Mol Carcinog. 2024 Jul;63(7):1248-1259. doi: 10.1002/mc.23721. Epub 2024 Apr 1.
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ENST00000534735 inhibits proliferation and migration, promotes apoptosis and pyroptosis of endometrial cancer via OSBPL3 through APMK/SIRT1/NF-κB pathway.ENST00000534735通过APMK/SIRT1/NF-κB途径经OSBPL3抑制子宫内膜癌的增殖和迁移,促进其凋亡和焦亡。
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Nanocarrier-Mediated Immunogenic Cell Death for Melanoma Treatment.纳米载体介导的免疫原性细胞死亡治疗黑色素瘤。
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Epigallocatechin gallate inhibits ovarian cancer cell growth and induces cell apoptosis via activation of FOXO3A.没食子酸表没食子儿茶素酯通过激活 FOXO3A 抑制卵巢癌细胞生长并诱导细胞凋亡。
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Cuproptosis-related lncRNAs ovarian cancer: Multi-omics analysis of molecular mechanisms and potential therapeutic targets.铜死亡相关长链非编码 RNA 与卵巢癌:分子机制的多组学分析及潜在治疗靶点。
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Inhibition of SF3B1 improves the immune microenvironment through pyroptosis and synergizes with αPDL1 in ovarian cancer.SF3B1 抑制通过细胞焦亡改善卵巢癌的免疫微环境,并与 αPDL1 协同作用。
Cell Death Dis. 2023 Nov 27;14(11):775. doi: 10.1038/s41419-023-06301-1.
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Ferroptosis and tumor immunity: In perspective of the major cell components in the tumor microenvironment.铁死亡与肿瘤免疫:从肿瘤微环境中主要细胞成分的角度看。
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Matrine induces ferroptosis in cervical cancer through activation of piezo1 channel.苦参碱通过激活Piezo1通道诱导宫颈癌铁死亡。
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ERRα promotes glycolytic metabolism and targets the NLRP3/caspase-1/GSDMD pathway to regulate pyroptosis in endometrial cancer.ERRα促进糖酵解代谢,并靶向NLRP3/半胱天冬酶-1/GSDMD通路来调节子宫内膜癌中的细胞焦亡。
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