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p53 controls the plasticity of mammary luminal progenitor cells downstream of Met signaling.

Aurélie ChicheAmandine Di-CiccoLaura Sesma-SanzLaura BressonPierre de la GrangeMarina A GlukhovaMarisa M FaraldoMarie-Ange Deugnier
Published in: Breast cancer research : BCR (2019)
Our study reveals a crosstalk between Met- and p53-mediated signaling pathways in the regulation of luminal progenitor function. In particular, it shows that neither p53 loss alone nor p53 loss combined with Met signaling activation caused an early detectable cell fate alteration in luminal progenitors. Conceivably, additional events are required to confer basal-specific characteristics to luminal-derived TNBCs.
Keyphrases
  • cell fate
  • tyrosine kinase
  • signaling pathway
  • epithelial mesenchymal transition