Please use this identifier to cite or link to this item: https://doi.org/10.3892/or.2011.1406
Title: Effect of triptolide on focal adhesion kinase and survival in MCF-7 breast cancer cells
Authors: Tan, B.-J. 
Tan, B.-H.
Chiu, G.N.C. 
Keywords: Breast cancer
Caspase
Focal adhesion kinase
Triptolide
Issue Date: Nov-2011
Citation: Tan, B.-J., Tan, B.-H., Chiu, G.N.C. (2011-11). Effect of triptolide on focal adhesion kinase and survival in MCF-7 breast cancer cells. Oncology Reports 26 (5) : 1315-1321. ScholarBank@NUS Repository. https://doi.org/10.3892/or.2011.1406
Abstract: Triptolide, a diterpene from Tripterygium wilfordii, has been shown to have potent anticancer activity, exerting its effects through multiple molecular targets and signaling pathways. Yet, its effect on focal adhesion kinase (FAK), a non-receptor tyrosine kinase overexpressed in breast cancer that regulates cellular adhesion and survival, has not been reported. The current study is the first to report on the effect of triptolide on FAK expression, cell adhesion and survival using MCF-7 breast cancer cells. Triptolide significantly reduced MCF-7 anchorage-independent growth in a concentration-dependent manner. Cell rounding and detachment from culture plates were observed as early as 8 h, with significant cell detachment observed after 24 h of triptolide treatment. The adhesion potential of triptolide-treated MCF-7 cells to Matrigel was also compromised. Triptolide induced concentration- and time-dependent cleavage of FAK and PARP, which was dependent on caspase activation. The pan-caspase inhibitor, zVAD-fmk, was the only inhibitor that could significantly reduce FAK and PARP cleavage and cell detachment. However, the presence of zVAD-fmk failed to significantly reverse triptolide-induced cell death. Finally, triptolide-induced FAK cleavage was specific to MCF-7 cells, as no cleaved FAK was observed in MDA-MB-231 cells. In conclusion, our data present the first evidence of triptolide-mediated induction of FAK cleavage that correlates with cell detachment and loss of adhesion potential to the extracellular matrix.
Source Title: Oncology Reports
URI: http://scholarbank.nus.edu.sg/handle/10635/105890
ISSN: 1021335X
DOI: 10.3892/or.2011.1406
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