癌细胞中的酸感应离子通道和下游信号:是否存在机理联系?

IF 2.9 4区 医学 Q2 PHYSIOLOGY
Stefan Gründer, Jakob Vanek, Karolos-Philippos Pissas
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引用次数: 0

摘要

越来越多的人认识到,肿瘤的酸性微环境对其演变和临床结果有影响。然而,我们对肿瘤细胞检测酸中毒的机制及其诱导的信号级联的了解仍然有限。酸感离子通道(ASIC)是质子的敏感受体,因此也是肿瘤细胞质子传感器的候选者。虽然在非转化组织中,它们的表达主要局限于神经元,但越来越多的研究报告称,ASICs 不仅在脑癌中异位表达,在乳腺癌和胰腺癌等不同癌肿中也有异位表达。然而,由于 ASIC 最为人们所熟知的是介导快速但短暂信号的脱敏离子受体,因此人们对它们如何触发细胞内信号级联还不甚了解。在这篇综述中,我们介绍了肿瘤的酸性微环境和 ASIC 的功能特性,指出了一些概念上的问题,总结了 ASIC 在不同癌症中的作用,并强调了它们在癌细胞中的作用机制方面的未决问题。最后,我们提出了一些指导原则,以确保 ASIC 在癌症中的研究有坚实的基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Acid-sensing ion channels and downstream signalling in cancer cells: is there a mechanistic link?

Acid-sensing ion channels and downstream signalling in cancer cells: is there a mechanistic link?

It is increasingly appreciated that the acidic microenvironment of a tumour contributes to its evolution and clinical outcomes. However, our understanding of the mechanisms by which tumour cells detect acidosis and the signalling cascades that it induces is still limited. Acid-sensing ion channels (ASICs) are sensitive receptors for protons; therefore, they are also candidates for proton sensors in tumour cells. Although in non-transformed tissue, their expression is mainly restricted to neurons, an increasing number of studies have reported ectopic expression of ASICs not only in brain cancer but also in different carcinomas, such as breast and pancreatic cancer. However, because ASICs are best known as desensitizing ionotropic receptors that mediate rapid but transient signalling, how they trigger intracellular signalling cascades is not well understood. In this review, we introduce the acidic microenvironment of tumours and the functional properties of ASICs, point out some conceptual problems, summarize reported roles of ASICs in different cancers, and highlight open questions on the mechanisms of their action in cancer cells. Finally, we propose guidelines to keep ASIC research in cancer on solid ground.

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来源期刊
CiteScore
8.80
自引率
2.20%
发文量
121
审稿时长
4-8 weeks
期刊介绍: Pflügers Archiv European Journal of Physiology publishes those results of original research that are seen as advancing the physiological sciences, especially those providing mechanistic insights into physiological functions at the molecular and cellular level, and clearly conveying a physiological message. Submissions are encouraged that deal with the evaluation of molecular and cellular mechanisms of disease, ideally resulting in translational research. Purely descriptive papers covering applied physiology or clinical papers will be excluded. Papers on methodological topics will be considered if they contribute to the development of novel tools for further investigation of (patho)physiological mechanisms.
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