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Published on: February 8, 2013
Differences between human breast cell lines in susceptibility towards growth inhibition by genistein
K Dampier1, E A Hudson, L M Howells
1MRC Toxicology Unit, University of Leicester, PO Box 138, Leicester LE1 9HN, UK.
Abstract:
Genistein is thought to contribute to the putative breast cancer preventive activity of soya. The mechanisms by which it arrests the growth of breast cells are incompletely understood. In order to explore generic features of the modulation of human breast cell growth by genistein, its effects on cell lines MCF-7, ZR-75.1, T47-D, MDA-MB 468, MDA-MB 231 and HBL 100 were compared. Genistein at 1 microM stimulated growth only in MCF-7 cells. At 10 microM it arrested the growth of all 6 cell types, however that of T47-D and HBL 100 cells only in medium with reduced (2%) fetal calf serum. Genistein induced apoptosis in only MDA-MB 468 cells. It arrested cells in the G2 stage of the cell cycle in all cell lines except ZR-75.1. Cells differed in their susceptibility towards inhibition by genistein of phorbol ester-induced proto-oncogene c-fos levels, transcription factor activator protein-1 (AP-1) activity and extracellular signal-regulated kinase (ERK) activity. Genistein augmented anisomycin-induced levels of proto-oncogene c-jun in ZR 75.1 and MCF-7 cells. The results suggest that induction of apoptosis, G2 cell cycle arrest and inhibition of c-fos expression, AP-1 transactivation and ERK phosphorylation may contribute to the growth-inhibitory effect of genistein in some breast cell types, but none of these effects of genistein constitutes a generic mode of growth-arresting action.
Insights
Genistein, found in soy, shows varied effects on breast cancer cells. While it can stimulate some cells, higher doses inhibit growth and cause cell cycle arrest, but not through a single universal mechanism.
Area of Science:
- Biochemistry
- Cell Biology
- Oncology
Background:
- Genistein from soy is linked to breast cancer prevention.
- Mechanisms of genistein's breast cell growth inhibition are not fully understood.
Purpose of the Study:
- To investigate genistein's effects on six human breast cell lines.
- To explore generic features of genistein's modulation of breast cell growth.
Main Methods:
- Compared genistein's effects (1 microM and 10 microM) on MCF-7, ZR-75.1, T47-D, MDA-MB 468, MDA-MB 231, and HBL 100 cell lines.
- Assessed genistein's impact on cell cycle progression, apoptosis, proto-oncogene expression (c-fos, c-jun), transcription factor activator protein-1 (AP-1) activity, and extracellular signal-regulated kinase (ERK) activity.
Main Results:
- Genistein (1 microM) stimulated MCF-7 cells; at 10 microM, it inhibited all six cell lines, with T47-D and HBL 100 requiring reduced serum.
- Genistein induced apoptosis in MDA-MB 468 cells and G2 cell cycle arrest in all lines except ZR-75.1.
- Differential susceptibility to genistein's inhibition of c-fos, AP-1, and ERK activity was observed across cell lines; c-jun was augmented in ZR 75.1 and MCF-7 cells.
Conclusions:
- Genistein's growth inhibition involves apoptosis, G2 cell cycle arrest, and modulation of signaling pathways like c-fos, AP-1, and ERK in specific breast cell types.
- No single mechanism universally explains genistein's growth-arresting action across all tested breast cell types.
