Is there a role for voltage-gated Na+ channels in the aggressiveness of breast cancer?

被引:0
作者
Rhana, P. [1 ,2 ]
Trivelato Junior, R. R. [1 ]
Beirao, P. S. L. [2 ]
Cruz, J. S. [2 ]
Rodrigues, A. L. P. [1 ]
机构
[1] Univ FUMEC, Lab Canc Mama, Fac Ciencias Humanas Sociais & Saude, Canais Ion & AMP Ciclico, Belo Horizonte, MG, Brazil
[2] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Bioquim & Imunol, Lab Membranas Excitveis & Biol Cardiovasc, Belo Horizonte, MG, Brazil
关键词
Breast cancer; Ion channels; Metastasis; Nav1.5; channel; RAT PROSTATE-CANCER; SODIUM-CHANNELS; ION CHANNELS; INVASIVE PROPERTIES; RNA INTERFERENCE; CELL-ADHESION; EXPRESSION; INVOLVEMENT; EXCHANGER; NAV1.5;
D O I
10.1590/1414-431X20176011
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Breast cancer is the most common cancer among women and its metastatic potential is responsible for numerous deaths. Thus, the need to find new targets for improving treatment, and even finding the cure, becomes increasingly greater. Ion channels are known to participate in several physiological functions, such as muscle contraction, cell volume regulation, immune response and cell proliferation. In breast cancer, different types of ion channels have been associated with tumorigenesis. Recently, voltage-gated Na+ channels (VGSC) have been implicated in the processes that lead to increased tumor aggressiveness. To explain this relationship, different theories, associated with pH changes, gene expression and intracellular Ca2+, have been proposed in an attempt to better understand the role of these ion channels in breast cancer. However, these theories are having difficulty being accepted because most of the findings are contrary to the present scientific knowledge. Several studies have shown that VGSC are related to different types of cancer, making them a promising pharmacological target against this debilitating disease. Molecular biology and cell electrophysiology have been used to look for new forms of treatment aiming to reduce aggressiveness and the disease progress.
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页数:10
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