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Cancer-Associated Intermediate Conductance Ca2+-Activated K+ Channel KCa3.1

机译:癌症相关的中间电导Ca2 +活化的k +通道Kca3.1

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摘要

Several tumor entities have been reported to overexpress KCa3.1 potassium channels due to epigenetic, transcriptional, or post-translational modifications. By modulating membrane potential, cell volume, or Ca2+ signaling, KCa3.1 has been proposed to exert pivotal oncogenic functions in tumorigenesis, malignant progression, metastasis, and therapy resistance. Moreover, KCa3.1 is expressed by tumor-promoting stroma cells such as fibroblasts and the tumor vasculature suggesting a role of KCa3.1 in the adaptation of the tumor microenvironment. Combined, this features KCa3.1 as a candidate target for innovative anti-cancer therapy. However, immune cells also express KCa3.1 thereby contributing to T cell activation. Thus, any strategy targeting KCa3.1 in anti-cancer therapy may also modulate anti-tumor immune activity and/or immunosuppression. The present review article highlights the potential of KCa3.1 as an anti-tumor target providing an overview of the current knowledge on its function in tumor pathogenesis with emphasis on vasculo- and angiogenesis as well as anti-cancer immune responses.
机译:已经报道了几种肿瘤实体对介质,转录或翻译后修饰引起的过表达KCA3.1钾通道。通过调节膜电位,细胞体积或CA2 +信号传导,已经提出了KCA3.1,以施加肿瘤发生,恶性进展,转移和治疗抵抗力的枢转致癌功能。此外,KCA3.1由肿瘤促进的基质细胞如成纤维细胞和肿瘤脉管系统表达,表明KCA3.1在适应肿瘤微环境中的作用。结合,这使得KCA3.1作为创新抗癌治疗的候选目标。然而,免疫细胞还表达KCA3.1,从而有助于T细胞活化。因此,靶向抗癌治疗中KCA3.1的任何策略也可以调节抗肿瘤免疫活性和/或免疫抑制。本综述文章突出了KCA3.1作为抗肿瘤目标的潜力,概述了目前关于其在肿瘤发病机制中的功能的知识,重点是血管和血管生成以及抗癌免疫应答。

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