研究动态
Articles below are published ahead of final publication in an issue. Please cite articles in the following format: authors, (year), title, journal, DOI.

癌症中的中电导钙激活钾通道 (KCa3.1):新兴作用和治疗潜力。

Intermediate conductance calcium-activated potassium channel (KCa3.1) in cancer: Emerging roles and therapeutic potentials.

发表日期:2024 Oct 11
作者: Nhung Thi Hong Van, Joo Hyun Nam
来源: BIOCHEMICAL PHARMACOLOGY

摘要:

KCa3.1 通道(也称为 KCNN4、IK1 或 SK4 通道)是一种中电导钙激活钾通道,可调节膜电位并维持钙稳态。最近,KCa3.1 通道因其在各种类型癌症中的不同作用而受到越来越多的关注。在癌细胞中,KCa3.1 通道调节关键过程,包括细胞增殖、细胞周期、迁移、侵袭、肿瘤微环境和治疗抵抗。此外,癌症中异常的 KCa3.1 表达可用于区分肿瘤和正常组织、对癌症分期进行分类并预测患者的生存结果。本综述全面考察了目前对 KCa3.1 通道对肿瘤形成、转移及其机制的贡献的认识。我们评估了 KCa3.1 作为癌症诊断和预后生物标志物的潜力。最后,我们讨论了 KCa3.1 调节剂在癌症治疗中应用的进展和挑战,并提出了克服这些障碍的方法。总之,这篇综述强调了这种离子通道作为癌症的有效治疗靶点和预后生物标志物的重要性。版权所有 © 2024 Elsevier Inc. 保留所有权利。
The KCa3.1 channel (also known as the KCNN4, IK1, or SK4 channel) is an intermediate-conductance calcium-activated potassium channel that regulates the membrane potential and maintains calcium homeostasis. Recently, KCa3.1 channels have attracted increasing attention because of their diverse roles in various types of cancers. In cancer cells, KCa3.1 channels regulate key processes, including cell proliferation, cell cycle, migration, invasion, tumor microenvironments, and therapy resistance. In addition, abnormal KCa3.1 expression in cancers is utilized to distinguish between tumor and normal tissues, classify cancer stages, and predict patient survival outcomes. This review comprehensively examines the current understanding of the contribution of KCa3.1 channels to tumor formation, metastasis, and its mechanisms. We evaluated the potential of KCa3.1 as a biomarker for cancer diagnosis and prognosis. Finally, we discuss the advances and challenges of applying KCa3.1 modulators in cancer treatment and propose approaches to overcome these obstacles. In summary, this review highlights the importance of this ion channel as a potent therapeutic target and prognostic biomarker of cancer.Copyright © 2024 Elsevier Inc. All rights reserved.