Sustained c-Jun-NH2-kinase activity promotes epithelial-mesenchymal transition, invasion, and survival of breast cancer cells by regulating extracellular signal-regulated kinase activation.

@article{Wang2010SustainedCA,
  title={Sustained c-Jun-NH2-kinase activity promotes epithelial-mesenchymal transition, invasion, and survival of breast cancer cells by regulating extracellular signal-regulated kinase activation.},
  author={Jinhua Wang and Isere Kuiatse and Adrian V. Lee and Jingxuan Pan and Armando Giuliano and Xiaojiang Cui},
  journal={Molecular cancer research : MCR},
  year={2010},
  volume={8 2},
  pages={266-77}
}
The c-Jun NH(2)-terminus kinase (JNK) mediates stress-induced apoptosis and the cytotoxic effect of anticancer therapies. Paradoxically, recent clinical studies indicate that elevated JNK activity in human breast cancer is associated with poor prognosis. Here, we show that overexpression of a constitutively active JNK in human breast cancer cells did not cause apoptosis, but actually induced cell migration and invasion, a morphologic change associated with epithelial-mesenchymal transition (EMT… CONTINUE READING
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