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dc.contributor.authorRajendran, P.
dc.contributor.authorOng, T.
dc.contributor.authorChen, L.
dc.contributor.authorLi, F.
dc.contributor.authorShanmugam, M.
dc.contributor.authorVali, S.
dc.contributor.authorAbbasi, T.
dc.contributor.authorKapoor, S.
dc.contributor.authorSharma, A.
dc.contributor.authorKumar, Alan Prem
dc.contributor.authorHui, K.
dc.contributor.authorSethi, G.
dc.date.accessioned2017-03-15T22:16:21Z
dc.date.available2017-03-15T22:16:21Z
dc.date.created2017-02-26T19:31:39Z
dc.date.issued2011
dc.identifier.citationRajendran, P. and Ong, T. and Chen, L. and Li, F. and Shanmugam, M. and Vali, S. and Abbasi, T. et al. 2011. Suppression of signal transducer and activator of transcription 3 activation by butein inhibits growth of human hepatocellular carcinoma in vivo. Clinical Cancer Research. 17 (6): pp. 1425-1439.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/49793
dc.identifier.doi10.1158/1078-0432.CCR-10-1123
dc.description.abstract

Purpose: Hepatocellular carcinoma (HCC) is the fifth most common malignancy worldwide and the third cause of global cancer mortality. Increasing evidence suggest that STAT3 is a critical mediator of oncogenic signaling in HCC and controls the expression of several genes involved in proliferation, survival, metastasis, and angiogenesis. Thus, the novel agents that can suppress STAT3 activation have potential for both prevention and treatment of HCC. Experimental Design: The effect of butein on STAT3 activation, associated protein kinases, STAT3-regulated gene products, cellular proliferation, and apoptosis was investigated. The in vivo effect of butein on the growth of human HCC xenograft tumors in male athymic nu/nu mice was also examined. Results: We tested an agent, butein, for its ability to suppress STAT3 activation in HCC cells and nude mice model along with prospectively testing the hypothesis of STAT3 inhibition in a virtual predictive functional proteomics tumor pathway technology platform. We found that butein inhibited both constitutive and inducible STAT3 activation in HCC cells. The suppression was mediated through the inhibition of activation of upstream kinases c-Src and Janus-activated kinase 2. Butein inhibited proliferation and significantly potentiated the apoptotic effects of paclitaxel and doxorubicin in HCC cells. When administered intraperitoneally, butein inhibited the growth of human HCC xenograft tumors in male athymic nu/nu mice. Conclusions: Overall, cumulative results from experimental and predictive studies suggest that butein exerts its antiproliferative and proapoptotic effects through suppression of STAT3 signaling in HCC both in vitro and in vivo.

dc.publisherAmerican Association Cancer Research
dc.titleSuppression of signal transducer and activator of transcription 3 activation by butein inhibits growth of human hepatocellular carcinoma in vivo
dc.typeJournal Article
dcterms.source.volume17
dcterms.source.number6
dcterms.source.startPage1425
dcterms.source.endPage1439
dcterms.source.issn1078-0432
dcterms.source.titleClinical Cancer Research
curtin.departmentSchool of Biomedical Sciences
curtin.accessStatusOpen access via publisher


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