HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Estrogens are not required for prolactin induced growth of MCF-7 human breast cancer cells.

Abstract
MCF-7 human breast cancer cells in continuous culture respond to the growth promoting activity of prolactin. Within 3 days of addition to culture medium in the presence of charcoal stripped fetal bovine serum which is depleted of bovine lactogens and estrogens, prolactin at 250 ng/ml promotes a 2- to 3-fold increase in cell number. When phenol red, which is a weak estrogen agonist, is also eliminated from the medium, the cells respond to prolactin to the same extent. When cells are grown for two generations in the presence of lactogen free, phenol red free, charcoal stripped serum, the prolactin induced response is even greater. Human and ovine prolactins are equipotent. The ability of the cells to bind lactogenic hormones remains unaltered by elimination of phenol red from the growth medium. These data indicate that prolactin alone is a mitogen for human breast cancer cells in long-term culture.
AuthorsB K Vonderhaar
JournalCancer letters (Cancer Lett) Vol. 47 Issue 1-2 Pg. 105-10 (Sep 15 1989) ISSN: 0304-3835 [Print] Ireland
PMID2636025 (Publication Type: Journal Article)
Chemical References
  • Estrogens
  • Prolactin
  • Placental Lactogen
  • Phenolsulfonphthalein
Topics
  • Breast Neoplasms (pathology)
  • Cell Division (drug effects)
  • Estrogens (pharmacology)
  • Female
  • Humans
  • Phenolsulfonphthalein (pharmacology)
  • Placental Lactogen (metabolism)
  • Prolactin (pharmacology)
  • Tumor Cells, Cultured

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: