From: Does consuming isoflavones reduce or increase breast cancer risk?
Compound | Effect | Test system* | ERα dependence | References |
---|---|---|---|---|
Genistein | Inhibition of tyrosine-specific protein kinase activity of EGFR, pp60v-src and pp110gag-fes | In vitro assay and A431 cells | Not assessed | [24] |
Genistein | Inhibition of the MEK5/ERK5/NF-κB pathway, leading to apoptosis | MDA-MB-231 cells | ERα-independent | [25] |
Genistein | G2/M-phase cell cycle arrest through activation of phosphorylated ERK1/2 | MDA-MB-231 cells | ERα-independent | [26] |
Genistein | Downregulation of the PI 3-kinase/Akt signaling pathway, leading to inhibition of estrogen-induced proliferation | MCF7 cells | ERα-dependent | [27] |
Genistein | Repression of HER2 protein expression, phosphorylation and HER2 promoter activity | BT-474 cells transfected with either ERα or ERβ | Both ERα-dependent and independent effects | [28] |
Genistein | Inhibition of proliferation and induction of apoptosis in BRCA1 mutant cells through p21CIP/WAF and Akt. Cells with wild-type BRCA1 were more resistant to effects of genistein | MDA-MB-231 cells (wild-type BRCA1); HCC1937, SUM149 and SUM1315 cells (mutated BRCA1) | Not assessed | [29] |
Genistein | Activation of cell growth through increased IGF-1 receptor gene expression | MCF-7 cells | Both ERα-dependent and independent effects | [30] |
Isoflavones | AR, PR and PPARγ binding and activation | In vitro ligand binding assay, yeast transcription activation assay | ERα-independent | [31] |