Dysregulated STAT1-SOCS1 control of JAK2 promotes mammary luminal progenitor cell survival and drives ERα+ tumorigenesis

@article{Chan2014DysregulatedSC,
  title={Dysregulated STAT1-SOCS1 control of JAK2 promotes mammary luminal progenitor cell survival and drives ERα+ tumorigenesis},
  author={Szeman Ruby Chan and Charles G. Rickert and William Vermi and Kathleen C. F. Sheehan and Cora D. Arthur and Julie A. Allen and Jordan M White and Jacques Archambault and Silvia Lonardi and Theresa M. McDevitt and Deepta Bhattacharya and Matthew V. Lorenzi and Donald Craig Allred and Robert D Schreiber},
  journal={Cell Death and Differentiation},
  year={2014},
  volume={21},
  pages={234-246}
}
We previously reported that STAT1 expression is frequently abrogated in human estrogen receptor-α-positive (ERα+) breast cancers and mice lacking STAT1 spontaneously develop ERα+ mammary tumors. However, the precise mechanism by which STAT1 suppresses mammary gland tumorigenesis has not been fully elucidated. Here we show that STAT1-deficient mammary epithelial cells (MECs) display persistent prolactin receptor (PrlR) signaling, resulting in activation of JAK2, STAT3 and STAT5A/5B, expansion of… CONTINUE READING
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