Regulation of death promoter Bak expression by cell density and 17 beta-estradiol in MCF-7 cells

Cancer Lett. 1998 Feb 13;124(1):47-52. doi: 10.1016/s0304-3835(97)00430-8.

Abstract

In the current study we examined the regulation of Bak, a death promoter of an apoptotic pathway, in the human breast cancer cell line MCF-7. We observed a time-dependent increase in both Bak mRNA and protein levels which appeared to correlate well with the increase in cell density. We also found that treatment of cells with 17beta-estradiol resulted in inhibition of the time-dependent increases in Bak mRNA and protein. The effects of estradiol appeared to be via estrogen receptor as treatment of cells with progesterone did not effect Bak expression. Our study provides additional molecular evidence for (1) a link between apoptosis pathways and cell-cell and/or cell-cell matrix interactions and (2) a role for estradiol in the modulation of signals between apoptosis pathways and cell-cell and/or cell-cell matrix interactions.

MeSH terms

  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Breast Neoplasms / ultrastructure
  • Cell Count
  • Estradiol / pharmacology*
  • Female
  • Humans
  • Membrane Proteins / biosynthesis*
  • Membrane Proteins / physiology
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • RNA, Messenger / metabolism
  • Receptors, Estrogen / physiology
  • Time Factors
  • Tumor Cells, Cultured
  • bcl-2 Homologous Antagonist-Killer Protein

Substances

  • BAK1 protein, human
  • Membrane Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Messenger
  • Receptors, Estrogen
  • bcl-2 Homologous Antagonist-Killer Protein
  • Estradiol