Please use this identifier to cite or link to this item: https://libjncir.jncasr.ac.in/xmlui/handle/10572/1931
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dc.contributor.authorWu, Min
dc.contributor.authorKim, Sahn-Ho
dc.contributor.authorDatta, Indrani
dc.contributor.authorLevin, Albert
dc.contributor.authorDyson, Gregory
dc.contributor.authorLi, Jing
dc.contributor.authorKaypee, Stephanie
dc.contributor.authorSwamy, M. Mahadeva
dc.contributor.authorGupta, Nilesh
dc.contributor.authorKwon, Ho Jeong
dc.contributor.authorMenon, Mani
dc.contributor.authorKundu, Tapas Kumar
dc.contributor.authorReddy, G. Prem-Veer
dc.date.accessioned2016-10-28T06:01:30Z-
dc.date.available2016-10-28T06:01:30Z-
dc.date.issued2015
dc.identifier.citationOncotargeten_US
dc.identifier.citation6en_US
dc.identifier.citation8en_US
dc.identifier.citationWu, M.; Kim, S. H.; Datta, I.; Levin, A.; Dyson, G.; Li, J.; Kaypee, S.; Swamy, M. M.; Gupta, N.; Kwon, H. J.; Menon, M.; Kundu, T. K.; Reddy, G. P. V., Hydrazinobenzoylcurcumin inhibits androgen receptor activity and growth of castration-resistant prostate cancer in mice. Oncotarget 2015, 6 (8), 6136-6150.en_US
dc.identifier.issn1949-2553
dc.identifier.urihttps://libjncir.jncasr.ac.in/xmlui/10572/1931-
dc.descriptionRestricted accessen_US
dc.description.abstractThere is a critical need for therapeutic agents that can target the amino-terminal domain (NTD) of androgen receptor (AR) for the treatment of castration-resistant prostate cancer (CRPC). Calmodulin (CaM) binds to the AR NTD and regulates AR activity. We discovered that Hydrazinobenzoylcurcumin (HBC), which binds exclusively to CaM, inhibited AR activity. HBC abrogated AR interaction with CaM, suppressed phosphorylation of AR Serine81, and blocked the binding of AR to androgen-response elements. RNA-Seq analysis identified 57 androgen-regulated genes whose expression was significantly (p <= 0.002) altered in HBC treated cells as compared to controls. Oncomine analysis revealed that genes repressed by HBC are those that are usually overexpressed in prostate cancer (PCa) and genes stimulated by HBC are those that are often down-regulated in PCa, suggesting a reversing effect of HBC on androgenregulated gene expression associated with PCa. Ingenuity Pathway Analysis revealed a role of HBC affected genes in cellular functions associated with proliferation and survival. HBC was readily absorbed into the systemic circulation and inhibited the growth of xenografted CRPC tumors in nude mice. These observations demonstrate that HBC inhibits AR activity by targeting the AR NTD and suggest potential usefulness of HBC for effective treatment of CRPC.en_US
dc.language.isoEnglishen_US
dc.publisherImpact Journals LLCen_US
dc.rights?Impact Journals LLC, 2015en_US
dc.subjectOncologyen_US
dc.subjectCell Biologyen_US
dc.subjectAndrogen receptoren_US
dc.subjectcalmodulinen_US
dc.subjectHydrazinobenzoylcurcuminen_US
dc.subjectCTK7Aen_US
dc.subjectcastration-resistant prostate canceren_US
dc.subjectSerine 81 Phosphorylationen_US
dc.subjectIn-Vivoen_US
dc.subjectCalmodulinen_US
dc.subjectCellsen_US
dc.subjectAren_US
dc.subjectActivationen_US
dc.subjectMechanismsen_US
dc.subjectTargeten_US
dc.subjectIdentificationen_US
dc.subjectProgressionen_US
dc.titleHydrazinobenzoylcurcumin inhibits androgen receptor activity and growth of castration-resistant prostate cancer in miceen_US
dc.typeArticleen_US
Appears in Collections:Research Papers (Tapas K. Kundu)

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