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={J. Wang and I. Kuiatse and A. Lee and Jingxuan Pan and A. Giuliano and X. Cui},
  journal={Molecular Cancer Research},
  year={2010},
  volume={8},
  pages={266 - 277}
}
  • J. Wang, I. Kuiatse, +3 authors X. Cui
  • Published 2010
  • Biology, Medicine
  • Molecular Cancer Research
  • The c-Jun NH2-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
    The transcription cofactor c-JUN mediates phenotype switching and BRAF inhibitor resistance in melanoma
    79
    Dexamethasone mediates pancreatic cancer progression by glucocorticoid receptor, TGFβ and JNK/AP-1
    10

    References

    Publications referenced by this paper.
    SHOWING 1-10 OF 72 REFERENCES
    Jun N-terminal kinase 1 regulates epithelial-to-mesenchymal transition induced by TGF-β1
    103
    C-Jun NH(2)-terminal kinase mediates proliferation and tumor growth of human prostate carcinoma.
    121