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CLC-3 channels in cancer (Review)

CLC-3 channels in cancer (Review) Ion channels are involved in regulating cell proliferation and apoptosis (programed cell death). Since increased cellular proliferation and inhibition of apoptosis are characteristic features of tumorigenesis, targeting ion channels is a promising strategy for treating cancer. CLC-3 is a member of the voltage-gated chloride channel superfamily and is expressed in many cancer cells. In the plasma membrane, CLC-3 functions as a chloride channel and is associated with cell proliferation and apoptosis. CLC-3 is also located in intracellular compartments, contributing to their acidity, which increases sequestration of drugs and leads to chemotherapy drug resistance. In this review, we summarize the recent findings concerning the involvement of CLC-3 in cancer and explore its potential in cancer therapy. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Oncology Reports Spandidos Publications

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Publisher
Spandidos Publications
Copyright
Copyright © Spandidos Publications
ISSN
1021-335X
eISSN
1791-2431
DOI
10.3892/or.2014.3615
pmid
25421907
Publisher site
See Article on Publisher Site

Abstract

Ion channels are involved in regulating cell proliferation and apoptosis (programed cell death). Since increased cellular proliferation and inhibition of apoptosis are characteristic features of tumorigenesis, targeting ion channels is a promising strategy for treating cancer. CLC-3 is a member of the voltage-gated chloride channel superfamily and is expressed in many cancer cells. In the plasma membrane, CLC-3 functions as a chloride channel and is associated with cell proliferation and apoptosis. CLC-3 is also located in intracellular compartments, contributing to their acidity, which increases sequestration of drugs and leads to chemotherapy drug resistance. In this review, we summarize the recent findings concerning the involvement of CLC-3 in cancer and explore its potential in cancer therapy.

Journal

Oncology ReportsSpandidos Publications

Published: Feb 1, 2015

References