Endogenous human prolactin and not exogenous human prolactin induces estrogen receptor α and prolactin receptor expression and increases estrogen responsiveness in breast cancer cells

The Prolactin Receptor Transactivation Domain Is Associated with Steroid Hormone Receptor Expression and Malignant Progression of Breast Cancer

“…50,55 These observations suggest that the transcriptional cross regulation of PRLr, ERa, and PR may contribute to their co-expression in breast cancer. However, although others have suggested that PRL may stimulate/contribute to ERa and PR transcription, 54,55 to our knowledge, this is the first report to determine the requirement for PRLr Y406 phosphorylation in steroid hormone receptor transcription. Thus, because the quantification and inhibition of both ER and ErbB2 are useful in the stratification and therapy of breast cancer, 90 similar strategies may be of utility for the PRLr.…”

“…The full list of genes that were up-or down-regulated in this analysis can be found in Supplemental Table S2. estrogen receptor (ERa) and the progesterone receptor (PR) was observed in many breast tumors. 50,52,53 Previous reports demonstrated that PRL up-regulated PR 50 and ERa in breast cancer cells 54,55 ; this induction was observed only after prolonged PRL stimulation (approximately 24 to 72 hours). We, therefore, examined the effects of prolonged PRL exposure on ERa/PR mRNA levels in PRLr or PRLrYDmut-expressing MCF7 cells.…”

Activation of the unliganded estrogen receptor by prolactin in breast cancer cells

“…Increased ERa levels are common in breast cancer (Fabris et al, 1987;Holst et al, 2007) and have been associated with aberrant promoter occupancy, increased gene expression and cell proliferation in the absence of hormonal stimulation (Fowler et al, 2004). Because it has been reported that PRL increases ERa levels in breast cancer cells (Shafie and Brooks, 1977;Gutzman et al, 2004a), the stimulatory effect of PRL on the ER target genes could be due to ERa induction. However, we did not observe increased receptor expression over the period in which PRL stimulates ER-dependent gene transcription.…”

“…One of the mechanisms of PRL and estrogen interaction is the cross-regulation of their receptors (Ormandy et al, 1997;Dong et al, 2006). It has been described that PRL increases ERa levels and E2 responsiveness in breast cancer cells (Shafie and Brooks, 1977;Gutzman et al, 2004a). In addition, both PRL and E2 increase ERK1/2 phosphorylation and cooperatively activate the transcription factor AP-1 (Gutzman et al, 2004b(Gutzman et al, , 2005.…”

JAK-STAT pathway in carcinogenesis: Is it relevant to cholangiocarcinoma progression?

“…Moreover, increased levels of correspondent ligands can be associated with JAK-STAT induced carcinogenesis: in animal models of prostate and mammary gland hyperplasia with local overexpression of Prl [33,34] ; in humans hyperprolactinemia is considered as a risk factor for breast and, probably, prostate cancer [35,36] ; overexpression of GH in transgenic mice leads to increased frequency of mammary adenocarcinoma [37] . A particular and essential role for neoplasia progression of autocrine production of Prl has been revealed [34,38] . Only autocrine, but not exocrine GH, is suggested to promote neoplasia [39][40][41] .…”