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本文引用的文献

1
Reducing αENaC expression in the kidney connecting tubule induces pseudohypoaldosteronism type 1 symptoms during K+ loading.在肾脏连接小管中降低αENaC表达会在钾负荷增加时诱发1型假性醛固酮减少症症状。
Am J Physiol Renal Physiol. 2016 Feb 15;310(4):F300-10. doi: 10.1152/ajprenal.00258.2015. Epub 2015 Nov 18.
2
Genes Regulating Epithelial Polarity Are Critical Suppressors of Esophageal Oncogenesis.调控上皮细胞极性的基因是抑制食管发生癌变的关键。
J Cancer. 2015 Jun 11;6(8):694-700. doi: 10.7150/jca.11709. eCollection 2015.
3
Regulation of the epithelial Na+ channel by the mTORC2/SGK1 pathway.mTORC2/SGK1 信号通路对上皮钠离子通道的调控
Nephrol Dial Transplant. 2016 Feb;31(2):200-5. doi: 10.1093/ndt/gfv270. Epub 2015 Jul 9.
4
Voltage-gated ion channels in cancer cell proliferation.癌细胞增殖中的电压门控离子通道
Cancers (Basel). 2015 May 22;7(2):849-75. doi: 10.3390/cancers7020813.
5
Cancer as a channelopathy: ion channels and pumps in tumor development and progression.癌症作为一种离子通道病:肿瘤发生与进展中的离子通道和泵
Front Cell Neurosci. 2015 Mar 17;9:86. doi: 10.3389/fncel.2015.00086. eCollection 2015.
6
Involvement of acid-sensing ion channel 1α in hepatic carcinoma cell migration and invasion.酸敏感离子通道1α在肝癌细胞迁移和侵袭中的作用
Tumour Biol. 2015 Jun;36(6):4309-17. doi: 10.1007/s13277-015-3070-6. Epub 2015 Jan 23.
7
Epoxyeicosatrienoic acids attenuating hypotonic-induced apoptosis of IMCD cells via γ-ENaC inhibition.
PLoS One. 2014 Apr 8;9(4):e94400. doi: 10.1371/journal.pone.0094400. eCollection 2014.
8
Ion channels in cancer: future perspectives and clinical potential.癌症中的离子通道:未来展望与临床潜力
Philos Trans R Soc Lond B Biol Sci. 2014 Feb 3;369(1638):20130108. doi: 10.1098/rstb.2013.0108. Print 2014 Mar 19.
9
Cystic fibrosis transmembrane regulator (CFTR) in human trophoblast BeWo cells and its relation to cell migration.人滋养层细胞中的囊性纤维化跨膜转导调节因子(CFTR)及其与细胞迁移的关系。
Placenta. 2014 Feb;35(2):92-8. doi: 10.1016/j.placenta.2013.12.004. Epub 2013 Dec 21.
10
The migratory capacity of human trophoblastic BeWo cells: effects of aldosterone and the epithelial sodium channel.人滋养层细胞 BeWo 的迁移能力:醛固酮和上皮钠通道的影响。
J Membr Biol. 2013 Mar;246(3):243-55. doi: 10.1007/s00232-013-9526-y. Epub 2013 Jan 26.

上皮钠通道/退化素在肿瘤发生发展中的作用

ENaC/DEG in Tumor Development and Progression.

作者信息

Liu Cui, Zhu Li-Li, Xu Si-Guang, Ji Hong-Long, Li Xiu-Min

机构信息

School of Nursing, Xinxiang Medical University, Xinxiang 453003, Henan Province, P. R. China.

Institute of Lung and Molecular Therapy, Xinxiang Medical University, Xinxiang 453003, Henan Province, P. R. China.

出版信息

J Cancer. 2016 Sep 13;7(13):1888-1891. doi: 10.7150/jca.15693. eCollection 2016.

DOI:10.7150/jca.15693
PMID:27698929
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5039373/
Abstract

The epithelial Na channel/degenerin (ENaC/DEG) superfamily, including the acid-sensing ion channels (ASICs), is characterized by a high degree of similarity in structure but highly diverse in physiological functions. These ion channels have been shown to be important in several physiological functions of normal epithelial cells, including salt homeostasis, fluid transportation and cell mobility. There is increasing evidence suggesting that ENaC/DEG channels are critically engaged in cancer cell biology, such as proliferation, migration, invasion and apoptosis, playing a role in tumor development and progression. In this review, we will discuss recent studies showing the role of ENaC and ASIC channels in epithelial cells and its relationship to the oncogenesis.

摘要

上皮钠通道/退化素(ENaC/DEG)超家族,包括酸敏感离子通道(ASICs),其特点是结构高度相似,但生理功能却高度多样。这些离子通道已被证明在正常上皮细胞的多种生理功能中发挥重要作用,包括盐稳态、液体运输和细胞迁移。越来越多的证据表明,ENaC/DEG通道在癌细胞生物学中起着关键作用,如增殖、迁移、侵袭和凋亡,在肿瘤的发生和发展中发挥作用。在本综述中,我们将讨论最近的研究,这些研究表明ENaC和ASIC通道在上皮细胞中的作用及其与肿瘤发生的关系。