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- Title
Inhibition of phosphorylated c-Met in rhabdomyosarcoma cell lines by a small molecule inhibitor SU11274.
- Authors
Jinxuan Hou; Jixin Dong; Lijun Sun; Liying Geng; Jing Wang; Jialin Zheng; Yan Li; Bridge, Julia; Hinrichs, Steven H.; Shi-Jian Ding; Hou, Jinxuan; Dong, Jixin; Sun, Lijun; Geng, Liying; Wang, Jing; Zheng, Jialin; Li, Yan; Ding, Shi-Jian
- Abstract
<bold>Background: </bold>c-Met is a receptor tyrosine kinase (RTK) that is over-expressed in a variety of cancers and involved in cell growth, invasion, metastasis and angiogenesis. In this study, we investigated the role of c-Met in rhabdomyosarcoma (RMS) using its small molecule inhibitor SU11274, which has been hypothesized to be a potential therapeutic target for RMS.<bold>Methods: </bold>The expression level of phosphorylated c-Met in RMS cell lines (RD, CW9019 and RH30) and tumor tissues was assessed by phospho-RTK array and immunohistochemistry, respectively. The inhibition effects of SU11274 on RMS cells were studied with regard to intracellular signaling, cell proliferation, cell cycle and cell migration.<bold>Results: </bold>A high level of phosphorylated c-Met was detected in 2 alveolar RMS cell lines (CW9019 and RH30) and 14 out of 24 RMS tissue samples, whereas relatively low levels of phospho-c-Met were observed in the embryonic RMS cell line (RD). The small molecule SU11274 could significantly reduce the phosphorylation of c-Met, resulting in inhibition of cell proliferation, G1 phase arrest of cell cycle and blocking of cell migration in CW9019 and RH30 cell lines.<bold>Conclusion: </bold>These results might support the role of c-Met in the development and progression of RMS. Furthermore, the inhibitor of c-Met, SU11274, could be an effective targeting therapy reagent for RMS, especially alveolar RMS.
- Subjects
PROTEIN-tyrosine kinases; RHABDOMYOSARCOMA; MUSCLE tumors; CELL growth; CELL lines
- Publication
Journal of Translational Medicine, 2011, Vol 9, Issue Suppl 1, p64
- ISSN
1479-5876
- Publication type
journal article
- DOI
10.1186/1479-5876-9-64