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Endogenous human prolactin amplifies the effects of estrogen on breast cancer.

Women's Health Weekly

| June 03, 2004 | COPYRIGHT 2004 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2004 JUN 3 - (NewsRx.com & NewsRx.net) -- Endogenous human prolactin amplifies the effects of estrogen on breast cancer.

According to a study from the United States, "prolactin (PRL) and estrogen act synergistically to increase mammary gland growth, development, and differentiation. Based on their roles in the normal gland, these hormones have been studied to determine their interactions in the development and progression of breast cancer. However, most studies have evaluated only endocrine PRL and did not take into account the recent discovery that PRL is synthesized by human mammary cells, permitting autocrine/paracrine activity. To examine the effects of this endogenous PRL, we engineered MCF7 cells to inducibly overexpress human prolactin (hPRL).

"Using this Tet-On MCF7hPRL cell line, we studied effects on cell growth, PRLR, estrogen receptor alpha (ERalpha) and progesterone receptor (PgR) levels, and estrogen target genes. Induced endogenous hPRL, but not exogenous hPRL, increased ERalpha levels as well as estrogen responsiveness in these cells, suggesting that effects on breast cancer development and progression by estrogen may be amplified by cross-regulation of ERalpha levels by endogenous hPRL," reported J.H. Gutzman and colleagues, University of Wisconsin-Madison, Department of Comparative Biosciences.

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