Differential responsiveness of MCF-7 human breast cancer cell line stocks to the pineal hormone, melatonin.

Journal Article (Journal Article)

The estrogen receptor (ER)-positive MCF-7 human breast cancer cell line has been used extensively for the study of estrogen-responsive human breast cancer. However, various levels of estrogen responsiveness have been described in different stocks of MCF-7 cells. Because we have previously shown that the pineal hormone, melatonin, inhibits proliferation of MCF-7 cells and can modulate ER expression and transactivation, we investigated if various stocks of MCF-7 cells exhibit a differential responsiveness to the anti-proliferative effects of melatonin and the possible mechanisms involved. The MCF-7 stocks (M, O, H) were examined for: (1) mitogenic response to estradiol; (2) steady-state ER mRNA levels; (3) expression of the mt1 melatonin membrane receptor; (4) growth inhibition by melatonin; and (5) melatonin's modulation of expression of the ER and the estrogen-regulated genes, PgR, TGFbeta and pS2. For all of these parameters, there was a stock-specific response which showed: MCF-7M > MCF-7O > MCF-7H. These results demonstrate that there are significant differences in the responsiveness of various stocks of MCF-7 breast cancer cells to the growth-inhibitory effects of melatonin which can be correlated with both the level of ER mRNA expression and the degree of estrogen-responsiveness. These findings suggest that not only may these differences have some impact on the cells' estrogen-response pathway, but also that the primary growth-inhibitory effects of melatonin are transduced through the membrane-associated G-protein coupled mt1 melatonin receptor.

Full Text

Duke Authors

Cited Authors

  • Ram, PT; Yuan, L; Dai, J; Kiefer, T; Klotz, DM; Spriggs, LL; Hill, SM

Published Date

  • May 2000

Published In

Volume / Issue

  • 28 / 4

Start / End Page

  • 210 - 218

PubMed ID

  • 10831156

International Standard Serial Number (ISSN)

  • 0742-3098

Digital Object Identifier (DOI)

  • 10.1034/j.1600-079x.2000.280403.x


  • eng

Conference Location

  • England