Melatonin inhibits estrogen receptor transactivation and cAMP levels in breast cancer cells.

Journal Article (Journal Article)

We have previously demonstrated that the pineal hormone, melatonin, can inhibit the growth of estrogen receptor-alpha (ERalpha)-positive breast cancer cells and suppress ERalpha gene transcription. To investigate the relationship between the estrogen response pathway and melatonin's growth inhibition, ERalpha-positive MCF-7 human breast cancer cells were transiently transfected with an estrogen response element (ERE) luciferase reporter construct and then treated with melatonin (10(-9)-10(-6) M) for 30 min followed by 10(-9) M 17-beta-estradiol (E2) or treated with each compound alone. Melatonin pre-treatment significantly reduced E2-induced ERalpha transactivation and ERalpha-ERE binding activity. We also conducted experiments to determine if melatonin modulates cAMP levels in MCF-7 cells. Melatonin inhibited the forskolin-induced and E2-induced elevation of cAMP levels by 57 and 45%, respectively. These data indicate that melatonin can act as a biological modifier to affect ERalpha transcriptional activity by regulating signal transduction pathways which impinge on the ERalpha and by altering E2-mediated ERalpha transactivation and ERalpha DNA binding activity.

Full Text

Duke Authors

Cited Authors

  • Kiefer, T; Ram, PT; Yuan, L; Hill, SM

Published Date

  • January 2002

Published In

Volume / Issue

  • 71 / 1

Start / End Page

  • 37 - 45

PubMed ID

  • 11859872

International Standard Serial Number (ISSN)

  • 0167-6806

Digital Object Identifier (DOI)

  • 10.1023/a:1013301408464


  • eng

Conference Location

  • Netherlands