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

• Published in: Cancer letters Vol. 124; no. 1; pp. 47 - 52
• Main Authors: Leung, Lai K, Do, Linh, T.Y. Wang, Thomas
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 13.02.1998; Elsevier
• Subjects: Apoptosis; Apoptosis - drug effects; Apoptosis - physiology; Bak; Bcl-2; bcl-2 Homologous Antagonist-Killer Protein; Biological and medical sciences; Breast cancer; Breast Neoplasms - metabolism; Breast Neoplasms - pathology; Breast Neoplasms - ultrastructure; Cell Count; Estradiol; Estradiol - pharmacology; Female; Gynecology. Andrology. Obstetrics; Humans; Mammary gland diseases; Medical sciences; Membrane Proteins - biosynthesis; Membrane Proteins - physiology; Proto-Oncogene Proteins c-bcl-2 - biosynthesis; Receptors, Estrogen - physiology; RNA, Messenger - metabolism; Time Factors; Tumor Cells, Cultured; Tumors; Bcl-2; Breast cancer; Bak; Estradiol; Apoptosis; Human; Gene product; Estrogen; 17β-Estradiol; Cell cell interaction; Malignant tumor; Gene expression; In vitro; Cell substratum interaction; Ovarian hormone; Mammary gland diseases; C-Onc gene; Established cell line; Mammary gland; Sex steroid hormone; Tumor cell; Tumor suppressor gene
• ISSN: 0304-3835; 1872-7980
• DOI: 10.1016/S0304-3835(97)00430-8

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 17 β-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.