Anti-breast cancer agents, quinolines, targeting gap junction

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dc.contributor.author Bernzweig, Julie
dc.contributor.author Heiniger, Brian
dc.contributor.author Prasain, Keshar
dc.contributor.author Lu, Jianyu
dc.contributor.author Hua, Duy H.
dc.contributor.author Nguyen, Thu A.
dc.date.accessioned 2012-06-05T14:57:16Z
dc.date.available 2012-06-05T14:57:16Z
dc.date.issued 2012-06-05
dc.date.issued Citation: Bernzweig, J., Heiniger, B., Prasain, K., Lu, J., Hua, D. H., & Nguyen, T. A. (2011). Anti-breast cancer agents, quinolines, targeting gap junction. Medicinal Chemistry, 7(5), 448-453.
dc.identifier.uri http://hdl.handle.net/2097/13917
dc.description.abstract Cancer cells exhibit many defects in cell communication that contribute to the loss of tissue homeostasis (excess cell proliferation, invasion, and metastasis). The process of cancer formation causes a disruption in cell homeostasis, affecting the ability to respond to extracellular signals, as well as triggering some intracellular events which alter gap junctional intercellular communication (GJIC). Previous research has shown that the first two generations of substituted quinolines have anti-cancer effects in human breast cancer cells. This report presents the synthesis and bioactivities of third generation substituted quinolines. Scrape load/dye transfer studies showed that 100 nM of PQ15, a third generation substituted quinoline, causes a 4.5-fold increase of gap junction activity in T47D breast cancer cells. Furthermore, a significant decrease of cell proliferation and viability was observed in the presence of 200 nM PQ15 compared to control. The expression of α-survivin was reduced to <18% in the treatment of 200 nM PQ15 compared to solvent alone. Alphasurvivin expression is upregulated in human cancers and associated with resistance to chemotherapy, suggesting that α-survivin prolongs the survival of cancer cells. Thus, it has been shown that substituted quinolines stimulate gap junction activity, decrease alpha survivin expression, and subsequently inhibit cancer cell growth. Our findings demonstrate that PQ15 has a promising role in exerting anti-cancer activity in human breast cancer cells. en_US
dc.relation.uri http://www.benthamdirect.org/pages/b_bypublication.php en_US
dc.subject Anti-cancer drugs en_US
dc.subject Breast cancer en_US
dc.subject Gap junctions en_US
dc.subject GJIC en_US
dc.subject 6-methoxy-4-methyl-8-[(4-quinolinylmethyl)amino]-5-(3- trifluoromethylphenyloxy)-quinoline en_US
dc.title Anti-breast cancer agents, quinolines, targeting gap junction en_US
dc.type Article (author version) en_US
dc.date.published 2011 en_US
dc.citation.epage 453 en_US
dc.citation.issue 5 en_US
dc.citation.jtitle Medicinal Chemistry en_US
dc.citation.spage 448 en_US
dc.citation.volume 7 en_US
dc.citation Bernzweig, J., Heiniger, B., Prasain, K., Lu, J., Hua, D. H., & Nguyen, T. A. (2011). Anti-breast cancer agents, quinolines, targeting gap junction. Medicinal Chemistry, 7(5), 448-453.
dc.contributor.authoreid duy en_US
dc.contributor.authoreid keshar en_US
dc.contributor.authoreid jianyulu en_US
dc.contributor.authoreid tanguyen en_US


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