作者: Christy R. Hagan , Andrea R. Daniel , Gwen E. Dressing , Carol A. Lange
DOI: 10.1016/J.MCE.2011.09.017
关键词:
摘要: Abstract Progesterone receptors (PR), in concert with peptide growth factor-initiated signaling pathways, initiate massive expansion of the epithelial cell compartment associated process alveologenesis developing mammary gland. PR-dependent events also contribute to inappropriate proliferation observed breast cancer. Notably, PR-B isoform-specific cross talk factor-driven pathways is required for proliferative actions progesterone. Indeed, PRs act as heavily phosphorylated transcription factor “sensors” mitogenic protein kinases that are often elevated and/or constitutively activated invasive cancers. In addition, phospho-PR-target genes frequently include components revealing a mechanism feed-forward confers increased responsiveness of, PR + mammary cells these same stimuli. Understanding mechanisms and isoform selectivity PR/kinase interactions may yield further insight into targeting altered networks other hormonally responsive cancers (i.e. lung, uterine ovarian) clinic. This review focuses on phosphorylation by PR-target gene selection lead proliferation.