Progesterone receptors act as sensors for mitogenic protein kinases in breast cancer models.
Progesterone receptors (PR), members of the nuclear receptor superfamily, function as ligand-activated transcription factors and initiators of c-Src kinase and mitogen-activated protein kinase signaling. Bidirectional cross-talk between PR and mitogenic protein kinases results in changes in PR post-translational modification, leading to alterations in PR transcriptional activity and promoter selectivity. PR-induced rapid activation of cytoplasmic protein kinases insures precise regulatory input to downstream cellular processes that are dependent upon nuclear PR, such as cell-cycle progression, and pro-survival signaling. Here, we review interactions between PR and mitogenic protein kinases and discuss the consequences of specific post-translational modifications on PR action in breast cancer cell-line models.
Department of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, MMC 806, Minneapolis, Minnesota 55455, USA.
Gwen E
GE
Dressing
Christy R
CR
Hagan
Todd P
TP
Knutson
Andrea R
AR
Daniel
Carol A
CA
Lange
D001943:Breast Neoplasms / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D011494:Protein Kinases / Q000378:metabolism*; D011499:Protein Processing, Post-Translational; D011980:Receptors, Progesterone / Q000502:physiology*; D015398:Signal Transduction
D011980:Receptors, Progesterone; D011494:Protein Kinases