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

  title={Endogenous human prolactin and not exogenous human prolactin induces estrogen receptor $\alpha$ and prolactin receptor expression and increases estrogen responsiveness in breast cancer cells},
  author={Jennifer H. Gutzman and Kristin K Miller and Linda A. Schuler},
  journal={The Journal of Steroid Biochemistry and Molecular Biology},

Ovarian hormones are not required for PRL-induced mammary tumorigenesis, but estrogen enhances neoplastic processes.

Findings indicate that PRL employs multiple mechanisms to promote mammary tumorigenesis, and chronic estrogen administration to ovx NRL-PRL females decreased the latency of both ERalpha-positive and -negative tumors.

Prolactin and estrogen enhance the activity of activating protein 1 in breast cancer cells: role of extracellularly regulated kinase 1/2-mediated signals to c-fos.

It is demonstrated that PRL and E2 cooperatively enhance the activity of AP-1 in MCF-7-derived cells and this activity may increase expression of many target genes that are critical for oncogenesis and may contribute to neoplastic progression.

Prolactin-growth factor crosstalk reduces mammary estrogen responsiveness despite elevated ERalpha expression.

Insight is provided into the interactions of PRL with growth factors during mammary oncogenesis and combinatorial approaches that may result in improved therapeutic efficacy are suggested.

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

It is shown that PRL is able to activate the unliganded estrogen receptor (ER) and ligand-independent ERα activation appears to be an important component of the proliferative and transcriptional actions of PRL in breast cancer cells.

Effects of 60 kDa prolactin and estradiol on metabolism and cell survival in cervical cancer: Co‑expression of their hormonal receptors during cancer progression.

The results revealed that ERα, ERβ, PRLR and Ki67 expression levels were increased during the progression of cancer, and the co‑expression of these receptors demonstrated the hormonal dependence of UCC.

Prolactin activates ERα in the absence of ligand in female mammary development and carcinogenesis in vivo.

It is demonstrated that PRL promotes pubertal ERα-dependent mammary ductal elongation and gene expression in the absence of estrogen, which are abrogated by the antiestrogen, ICI 182,780 (ICI).

Regulation of Prolactin Receptor Levels and Activity in Breast Cancer

The principle focus of this review is on the regulation of PRLr expression and activity in breast cancer with a brief overview of different isoforms of PR Lr, their expression, signaling capabilities and the biological outcomes ofPRL/PRLr signaling.

Prolactin and breast cancer risk.




Prolactin mediation of estrogen-induced changes in mammary tissue estrogen and progesterone receptors.

It is demonstrated that, of PRL and estradiol, PRL is the dominant factor in eliciting ER activity in mouse mammary gland.

Prolactin induces ERα-positive and ERα-negative mammary cancer in transgenic mice

These studies provide a mouse model of hormonally dependent breast cancer, and, perhaps most strikingly, a model in which some neoplasms retain ERα, as occurs in the human disease.

Biological and clinical aspects of prolactin receptors (PRL-R) in human breast cancer

Effect of prolactin on growth and the estrogen receptor level of human breast cancer cells (MCF-7).

The intracellular specific 17beta-estradiol binding in the human breast cancer cell line, MCF-7, was shown to be modified by Prolactin, and the possible mechanism implicating prolactin as an effector of differentiation and growth of MCF -7 cells is discussed.

Expression of prolactin and its receptor in human breast carcinoma.

Given the widespread expression of PRL-PRLr in breast cancer, pharmacological interventions aimed at the inhibition of function of this growth regulatory receptor complex may be of considerable utility in the therapy of this disease.

Expression of prolactin and prolactin receptor in human breast carcinoma. Evidence for an autocrine/paracrine loop.

Analysis of data indicates that prolactin may participate in an autocrine/paracrine stimulatory loop within breast tissues and suggest a role for this growth factor in the pathogenesis of breast cancer.

Prolactin Overexpression by MDA-MB-435 Human Breast Cancer Cells Accelerates Tumor Growth

Data support a role for breast PRL as a growth/anti-apoptotic factor and suggest that it may serve as a novel therapeutic target for the treatment of breast cancer.

Functional activity of ectopically expressed estrogen receptor is not sufficient for estrogen-mediated cyclin D1 expression.

The ability of estrogen to regulate cyclin D1 expression in estrogen receptor-negative breast cancer cells and nontransformed human keratinocytes stably expressing the estrogen receptor was characterized and it was found that estrogen receptor function alone is not sufficient for estrogen-dependent cyclinD1 expression and proliferation.

Prolactin synthesis and secretion by human breast cancer cells.

The addition of a panel of anti-human Prl mAbs to T47Dco and MCF7 human breast adenocarcinoma cells suggests that human breast cancer cells synthesize and secrete biologically active Prl.