June 21, 1999 Acting as a chemical attractant, the hormone prolactin stimulates the coordinated movement of breast cancer cells in culture, according to new findings from researchers at the University of Pennsylvania Medical Center. Using time-lapse video microscopy, the scientists were able to show that breast cancer cells will move toward a prolactin source in cell culture and even cross a membranous barrier to reach the source.
Also revealed was that the prolactin-induced motion of breast cancer cells is accompanied by corresponding changes in the cellular machinery responsible for motion. The experiments demonstrated that prolactin triggers the formation of actin filaments and lamellipodia, features that can be thought of as the muscles and feet, respectively, of the cell.
Prolactin normally functions to prompt the growth and maturation of breast tissues as a prelude to lactation during pregnancy. Data from several laboratories, however, including the Penn team's, have indicated that prolactin also stimulates the progression of breast cancer, although precise details of its action have been elusive. The current study describes a novel prolactin-mediated mechanism that may be a significant driver behind breast-cancer metastasis and suggests new directions for the development of drugs that might block disease progression.
"Since breast cancer mortality is a consequence of the movement, or metastasis, of the cancer from mammary tissues to other sites in the body, this study provides new insights into how prolactin may stimulate disease progression," says Charles V. Clevenger, MD, PhD, senior researcher on the study and an assistant professor of pathology and laboratory medicine. "We're using this information in our laboratory to try to develop novel pharmaceutical agents that might be useful in the treatment of breast cancer."
Lead researcher Marcela Maus, a graduate student in Clevenger's laboratory, presented data from the study at the 81st annual meeting of The Endocrine Society in San Diego, CA, on June 13, 1999.
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