Molecular mechanisms of TRP regulation in tumor growth and metastasis

被引：98

作者：

Gkika, Dimitra

Prevarskaya, Natalia ^{[1
]}

机构：

[1] Equipe Labellisee Ligue Natl Contre Canc, INSERM, U800, F-59656 Villeneuve Dascq, France

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2009年 / 1793卷 / 06期

关键词：

Ion channel; Cancer; Transcription; Hormonal regulation; Growth factor; Isoform; TRP; CANCER-CELL-PROLIFERATION; EPITHELIAL CA2+ CHANNELS; HUMAN PROSTATE-CANCER; FACTOR-I; GENE-EXPRESSION; CATION CHANNELS; ENDOPLASMIC-RETICULUM; VASCULAR-PERMEABILITY; MELANOMA METASTASIS; CALCIUM-ABSORPTION;

D O I：

10.1016/j.bbamcr.2008.11.010

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Transient Receptor Potential (TRP) channels modulate intracellular Ca2+ concentrations, consequently affecting both cell death and proliferation. It is not, therefore, surprising that the membrane expression of some TRP channels is altered during tumor growth and metastasis. These variations in channel abundance are due to TRP regulation on the transcriptional, translational, and targeting levels. This article mainly reviews the transcriptional mechanisms modulating TRP expression during tumorigenesis, involving hormones, growth factors, and alternative splicing. (C) 2008 Elsevier B.V. All rights reserved.

引用

页码：953 / 958

页数：6

共 92 条

[71] Functional expression of the epithelial Ca2+ channels (TRPV5 and TRPV6) requires association of the S100A10-annexin 2 complex [J].