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重新利用阳离子两亲性药物及其衍生物以引发溶酶体细胞死亡用于癌症治疗。

Repurposing Cationic Amphiphilic Drugs and Derivatives to Engage Lysosomal Cell Death in Cancer Treatment.

作者信息

Hu Michelle, Carraway Kermit L

机构信息

Department of Biochemistry and Molecular Medicine, UC Davis School of Medicine, Sacramento, CA, United States.

UC Davis Comprehensive Cancer Center, UC Davis School of Medicine, Sacramento, CA, United States.

出版信息

Front Oncol. 2020 Dec 10;10:605361. doi: 10.3389/fonc.2020.605361. eCollection 2020.

Abstract

A major confounding issue in the successful treatment of cancer is the existence of tumor cell populations that resist therapeutic agents and regimens. While tremendous effort has gone into understanding the biochemical mechanisms underlying resistance to each traditional and targeted therapeutic, a broader approach to the problem may emerge from the recognition that existing anti-cancer agents elicit their cytotoxic effects almost exclusively through apoptosis. Considering the myriad mechanisms cancer cells employ to subvert apoptotic death, an attractive alternative approach would leverage programmed necrotic mechanisms to side-step therapeutic resistance to apoptosis-inducing agents. Lysosomal cell death (LCD) is a programmed necrotic cell death mechanism that is engaged upon the compromise of the limiting membrane of the lysosome, a process called lysosomal membrane permeabilization (LMP). The release of lysosomal components into the cytosol upon LMP triggers biochemical cascades that lead to plasma membrane rupture and necrotic cell death. Interestingly, the process of cellular transformation appears to render the limiting lysosomal membranes of tumor cells more fragile than non-transformed cells, offering a potential therapeutic window for drug development. Here we outline the concepts of LMP and LCD, and discuss strategies for the development of agents to engage these processes. Importantly, the potential exists for existing cationic amphiphilic drugs such as antidepressants, antibiotics, antiarrhythmics, and diuretics to be repurposed to engage LCD within therapy-resistant tumor cell populations.

摘要

癌症成功治疗中的一个主要混杂问题是存在对治疗药物和方案产生抗性的肿瘤细胞群体。尽管人们付出了巨大努力来理解每种传统治疗和靶向治疗抗性背后的生化机制,但从认识到现有抗癌药物几乎完全通过凋亡引发细胞毒性作用这一点来看,可能会出现一种更广泛的解决该问题的方法。考虑到癌细胞用于规避凋亡死亡的无数机制,一种有吸引力的替代方法是利用程序性坏死机制来避开对凋亡诱导剂的治疗抗性。溶酶体细胞死亡(LCD)是一种程序性坏死性细胞死亡机制,它在溶酶体的限制膜受损时启动,这一过程称为溶酶体膜通透性增加(LMP)。LMP时溶酶体成分释放到细胞质中会触发生化级联反应,导致质膜破裂和坏死性细胞死亡。有趣的是,细胞转化过程似乎使肿瘤细胞的限制溶酶体膜比未转化细胞更脆弱,这为药物开发提供了一个潜在的治疗窗口。在这里,我们概述了LMP和LCD的概念,并讨论了开发参与这些过程的药物的策略。重要的是,现有阳离子两亲性药物如抗抑郁药、抗生素、抗心律失常药和利尿剂有可能被重新用于在治疗抗性肿瘤细胞群体中引发LCD。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc41/7793984/658f1999433e/fonc-10-605361-g001.jpg

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