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Gap Junction Enhancer Potentiates Cytotoxicity of Cisplatin in Breast Cancer Cells | OMICS International | Abstract
ISSN: 1948-5956

Journal of Cancer Science & Therapy
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Research Article

Gap Junction Enhancer Potentiates Cytotoxicity of Cisplatin in Breast Cancer Cells

Ying Ding1 and Thu Annelise Nguyen2*

1Department of Biochemistry, Kansas State University, Manhattan, Kansas, USA

2Department of Diagnostic Medicine/ Pathobiology, Kansas State University, Manhattan, Kansas, USA

*Corresponding Author:
Thu Annelise Nguyen
Kansas State University, K244 Mosier Hall
1800 Denison Avenue, Manhattan, KS 66506, USA
Tel: 785-532-4429
Fax: 785-532-4039
E-mail: [email protected]

Received date: September 20, 2012; Accepted date: October 23, 2012; Published date: October 25, 2012

Citation: Ding Y, Nguyen TA (2012) Gap Junction Enhancer Potentiates Cytotoxicity of Cisplatin in Breast Cancer Cells. J Cancer Sci Ther 4: 371-378. doi: 10.4172/1948-5956.1000170

Copyright: © 2012 Ding Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Cisplatin is one of the most widely used anti-cancer drugs due to its ability to damage DNA and induce apoptosis. However, increasing reports of side effects and drug resistance indicate the limitation of cisplatin in cancer therapeutics. Recent studies showed that inhibition of gap junctions diminishes the cytotoxic effect and contributes to drug resistance. Therefore, identification of molecules that counteract gap junctional inhibition without decreasing the anti-cancer effect of cisplatin could be used in combinational treatment, potentiating cisplatin efficacy and preventing resistance. This study investigates the effects of combinational treatment of cisplatin and PQ1, a gap junction enhancer, in T47D breast cancer cells. Our results showed that combinational treatment of PQ1 and cisplatin increased gap junctional intercellular communication (GJIC) as well as expressions of connexins (Cx26, Cx32 and Cx43), and subsequently decreased cell viability. Ki67, a proliferation marker, was decreased by 75% with combinational treatment. Expressions of pro-apoptotic factors (cleaved caspase-3/-8/-9 and bax) were increased by the combinational treatment with PQ1 and cisplatin; whereas, the pro-survival factor, bcl-2, was decreased by the combinational treatment. Our study demonstrates for the first time that the combinational treatment with gap junction enhancers can counteract cisplatin induced inhibition of gap junctional intercellular communication and reduction of connexin expression, thereby increasing the efficacy of cisplatin in cancer cells.