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김은희

Kim, Eunhee
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Involvement of c-Src kinase in the regulation of TGF-beta 1-induced apoptosis

Author(s)
Park, SSEom, YWKim, EunheeLee, JHMin, DSKim, SKim, SJChoi, KS
Issued Date
2004-08
DOI
10.1038/sj.onc.1207856
URI
https://scholarworks.unist.ac.kr/handle/201301/20187
Fulltext
http://www.nature.com/onc/journal/v23/n37/full/1207856a.html
Citation
ONCOGENE, v.23, no.37, pp.6272 - 6281
Abstract
Transforming growth factor-beta1 (TGF-beta1) is a potent inducer of apoptosis in normal hepatocytes, and acquiring resistance to TGF-beta1 may be a critical step in the development of hepatocellular carcinoma (HCC). In this study, we investigated the possible involvement of c-Src in the regulation of TGF-beta1-induced apoptosis. TGF-beta1 induced transient activation of c-Src and its subsequent caspase-mediated degradation concomitant with cell death in FaO hepatoma cells, which are sensitive to TGF-beta1. In response to TGF-beta1, activated c-Src was translocated into the cytoplasmic membrane, then relocated to the nuclei of apoptotic cells during its cleavage. In TGF-beta1-induced apoptotic cells, c-Src maintained its tight association with p85 FAK fragment cleaved by caspases, possibly contributing to focal adhesion disassembly. TGF-beta1-induced apoptosis was enhanced by either inhibition of c-Src activity using PP1 or PP2, or by overexpression of dominant-negative c-Src. In contrast, overexpression of constitutively active c-Src inhibited apoptosis suppressing TGF-beta1-induced activation of p38, JNK and caspases. In many HCC cell lines resistant to TGF-beta1, enhanced c-Src activity was detected. We hypothesize that activated c-Src in HCC may contribute to resistance against the apoptotic and/or antiproliferative properties of TGF-beta1
Publisher
NATURE PUBLISHING GROUP
ISSN
0950-9232

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