TRIP13: A promising cancer immunotherapy target

Cancer Innovation Pub Date : 2024-10-11 DOI:10.1002/cai2.147
Shengnan Jing, Liya Zhao, Liwen Zhao, Yong-Jing Gao, Tianzhen He
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引用次数: 0

Abstract

The tumor microenvironment (TME) facilitates tumor development through intricate intercellular signaling, thereby supporting tumor growth and suppressing the immune response. Thyroid hormone receptor interactor 13 (TRIP13), an AAA+ ATPase, modulates the conformation of client macromolecules, consequently influencing cellular signaling pathways. TRIP13 has been implicated in processes such as proliferation, invasion, migration, and metastasis during tumor progression. Recent studies have revealed that TRIP13 also plays a role in immune response suppression within the TME. Thus, inhibiting these functions of TRIP13 could potentially enhance immune responses and improve the efficacy of immune checkpoint inhibition. This review summarizes the recent research progress of TRIP13 and discusses the potential of targeting TRIP13 to improve immune-based therapies for patients with cancer.

Abstract Image

TRIP13:前景广阔的癌症免疫疗法靶点
肿瘤微环境(TME)通过错综复杂的细胞间信号传递促进肿瘤发生,从而支持肿瘤生长并抑制免疫反应。甲状腺激素受体互作因子 13(TRIP13)是一种 AAA+ ATP 酶,可调节客户大分子的构象,从而影响细胞信号通路。TRIP13 与肿瘤进展过程中的增殖、侵袭、迁移和转移等过程有关。最近的研究发现,TRIP13 还在 TME 内的免疫反应抑制中发挥作用。因此,抑制TRIP13的这些功能有可能增强免疫反应,提高免疫检查点抑制剂的疗效。本综述总结了 TRIP13 的最新研究进展,并探讨了靶向 TRIP13 改善癌症患者免疫疗法的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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