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肿瘤细胞中的 K(+) 通道与细胞周期进程。

K(+) channels and cell cycle progression in tumor cells.

机构信息

Laboratory of Cellular and Molecular Physiology EA4667, SFR CAP-SANTE FED 4231, UFR Sciences, University of Picardie Jules Verne Amiens, France.

出版信息

Front Physiol. 2013 Aug 20;4:220. doi: 10.3389/fphys.2013.00220. eCollection 2013.

DOI:10.3389/fphys.2013.00220
PMID:23970866
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3747328/
Abstract

K(+) ions play a major role in many cellular processes. The deregulation of K(+) signaling is associated with a variety of diseases such as hypertension, atherosclerosis, or diabetes. K(+) ions are important for setting the membrane potential, the driving force for Ca(2+) influx, and regulate volume of growing cells. Moreover, it is increasingly recognized that K(+) channels control cell proliferation through a novel signaling mechanisms triggered and modulated independently of ion fluxes. In cancer, aberrant expression, regulation and/or sublocalization of K(+) channels can alter the downstream signals that converge on the cell cycle machinery. Various K(+) channels are involved in cell cycle progression and are needed only at particular stages of the cell cycle. Consistent with this idea, the expression of Eag1 and HERG channels fluctuate along the cell cycle. Despite of acquired knowledge, our understanding of K(+) channels functioning in cancer cells requires further studies. These include identifying the molecular mechanisms controlling the cell cycle machinery. By understanding how K(+) channels regulate cell cycle progression in cancer cells, we will gain insights into how cancer cells subvert the need for K(+) signal and its downstream targets to proliferate.

摘要

钾离子在许多细胞过程中起着重要作用。钾信号的失调与多种疾病有关,如高血压、动脉粥样硬化或糖尿病。钾离子对于设定膜电位、钙离子内流的驱动力以及调节生长细胞的体积非常重要。此外,越来越多的人认识到,钾通道通过一种新的信号机制控制细胞增殖,这种信号机制独立于离子流触发和调节。在癌症中,钾通道的异常表达、调节和/或亚定位可以改变下游信号,这些信号汇集到细胞周期机制上。各种钾通道参与细胞周期的进展,并且只在细胞周期的特定阶段需要。与这一观点一致,Eag1 和 HERG 通道的表达沿细胞周期波动。尽管已经有了相关的知识,但我们对癌细胞中钾通道功能的理解还需要进一步的研究。这些研究包括确定控制细胞周期机制的分子机制。通过了解钾通道如何调节癌细胞的细胞周期进程,我们将深入了解癌细胞如何颠覆对钾信号及其下游靶标的需求以进行增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7fa/3747328/524ae4e8149d/fphys-04-00220-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7fa/3747328/524ae4e8149d/fphys-04-00220-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7fa/3747328/524ae4e8149d/fphys-04-00220-g0001.jpg

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