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Sophoraflavanone G induces apoptosis of human cancer cells by targeting upstream signals of STATs

Authors
 Byung-Hak Kim ; Cheolhee Won ; Myoung-Hwan Kim ; Sang-Kyu Ye ; Dong-Sup Lee ; Chang Seok Lee ; Haeri Lee ; Songhee Han ; Kum Hee Noh ; Jung Sook Choi ; Yun-Han Lee 
Citation
 Biochemical Pharmacology, Vol.86(7) : 950~959, 2013 
Journal Title
 Biochemical Pharmacology 
ISSN
 0006-2952 
Issue Date
2013
Abstract
Aberrantly activated signal transducer and activator of transcription (STAT) proteins are implicated with human cancers and represent essential roles for cancer cell survival and proliferation. Therefore, the development of small-molecule inhibitors of STAT signaling bearing pharmacological activity has therapeutic potential for the treatment of human cancers. In this study, we identified sophoraflavanone G as a novel small-molecule inhibitor of STAT signaling in human cancer cells. Sophoraflavanone G inhibited tyrosine phosphorylation of STAT proteins in Hodgkin's lymphoma and tyrosine phosphorylation of STAT3 in solid cancer cells by inhibiting phosphorylation of the Janus kinase (JAK) proteins, Src family tyrosine kinases, such as Lyn and Src, Akt, and ERK1/2. In addition, sophoraflavanone G inhibited STAT5 phosphorylation in murine-bone-marrow-derived pro-B cells transfected with translocated Ets Leukemia (TEL)-JAKs and cytokine-induced rat pre-T lymphoma cells, as well as STAT5b reporter activity in TEL-JAKs and STAT5b reporter systems. Sophoraflavanone G also inhibited nuclear factor-κB (NF-κB) signaling in multiple myeloma cells. Furthermore, sophoraflavanone G inhibited cancer cell proliferation and induced apoptosis by regulating the expression of apoptotic and anti-apoptotic proteins. Our data suggest that sophoraflavanone G is a novel small-molecule inhibitor of STAT signaling by targeting upstream signals of STATs that may have therapeutic potential for cancers caused by persistently activated STAT proteins.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/88177
DOI
10.1016/j.bcp.2013.08.009
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Radiation Oncology
Yonsei Authors
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Link
 http://www.sciencedirect.com/science/article/pii/S0006295213004954
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