期刊
CANCER LETTERS
卷 292, 期 2, 页码 197-207出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2009.12.003
关键词
STAT3; JAK2; Diosgenin; Hepatocellular carcinoma; Apoptosis
类别
资金
- Department of Research and Technology, Singapore
- Biomedical Research Council of Singapore
- National Medical Research Council of Singapore
- Singapore Millennium Foundation
Constitutive activation of STAT3 has been shown in several human cancers and transformed cell lines including hepatocellular carcinoma (HCC). In the present report, we investigated whether diosgenin, a steroidal saponin isolated from fenugreek can modulate the STAT3 signaling pathway We found that diosgenin inhibited both constitutive and inducible activation of STAT3 with no effect on STAT5 The activation of c-Src, JAK1 and JAK2 implicated in STAT3 activation, were also suppressed by this saponin Pervanadate reversed the diosgenin-induced downregulation of STAT3, suggesting the involvement of a protein tyrosine phosphatase Indeed, we found that diosgenin can induce the expression of Src homology 2 phosphatase 2 (SH-PTP2) that correlated with downregulation of constitutive STAT3 activation Diosgenin also downregulated the expression of various STAT3-regulated gene products, inhibited proliferation and potentiated the apoptotic effects of paclitaxel and doxorubicin Overall, these results suggest that diosgenin is a novel blocker of the STAT3 activation pathway. with a potential role in the treatment of HCC and other cancers (C) 2009 Elsevier Ireland Ltd All rights reserved.
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