Excess PLAC8 promotes an unconventional ERK2-dependent EMT in colon cancer.

@article{Li2014ExcessPP,
  title={Excess PLAC8 promotes an unconventional ERK2-dependent EMT in colon cancer.},
  author={Cunxi Li and Haiting Ma and Yang Wang and Zheng Zheng Cao and Ramona Graves-Deal and Anne Elizabeth Powell and Alina Starchenko and Gregory Daniel Ayers and M. Kay Washington and Vidya Kamath and Keyur M. Desai and Michael J. Gerdes and Lila Solnica-Krezel and Robert J Coffey},
  journal={The Journal of clinical investigation},
  year={2014},
  volume={124 5},
  pages={
          2172-87
        }
}
The epithelial-to-mesenchymal transition (EMT) transcriptional program is characterized by repression of E-cadherin (CDH1) and induction of N-cadherin (CDH2), and mesenchymal genes like vimentin (VIM). Placenta-specific 8 (PLAC8) has been implicated in colon cancer; however, how PLAC8 contributes to disease is unknown, and endogenous PLAC8 protein has not been studied. We analyzed zebrafish and human tissues and found that endogenous PLAC8 localizes to the apical domain of differentiated… CONTINUE READING

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