| Norcantharidin induces melanoma cell apoptosis through activation of TR3 dependent pathway. | |
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MedLine Citation:
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PMID: 22123174 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Norcantharidin (NCTD) has been reported to induce tumor cell apoptosis. However, the underlying mechanism behinds its antitumor effect remains elusive. We have previously shown that TR3 expression is significantly decreased in metastatic melanomas and involved in melanoma cell apoptosis. In this study, we showed that NCTD inhibited melanoma cell proliferation and induced apoptosis in a dose related manner. NCTD induced translocation of TR3 from nucleus to mitochondria where it co-localized with Bcl-2 in melanoma cells. NCTD also increased cytochome c release from mitochondria to the cytoplasm. These changes were accompanied by increased expression of Bax and cleaved caspase-3 along with decreased expression of Bcl2 and NF-B2. The effects of NCTD were inhibited by knockdown of TR3 expression using TR3 specific shRNA in melanoma cells. Furthermore, NCTD significantly decreased tumor volume and improved survival of Tyr::CreER; BRAFCa/+; Ptenlox/lox transgenic mice. Our data indicates that NCTD inhibits melanoma growth by inducing tumor cell apoptosis via activation of a TR3 dependent pathway. These results suggest that NCTD is a potential therapeutic agent for melanoma. |
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Authors:
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Shujing Liu; Hong Yu; Suresh M Kumar; James S Martin; Zhanyong Bing; Weiqi Sheng; Marcus Bosenberg; Xiaowei Xu |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-12-01 |
Journal Detail:
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Title: Cancer biology & therapy Volume: 12 ISSN: 1555-8576 ISO Abbreviation: - Publication Date: 2011 Dec |
Date Detail:
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Created Date: 2011-11-29 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101137842 Medline TA: Cancer Biol Ther Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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University of Pennsylvania School of Medicine, Philadelphia, PA, USA. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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