one can conclude that ERβ has an overall antiproliferative effect, thereby inhibiting cancer cell
proliferation and antagonizing ERα function in the breast
HRT with estrogen alone did not increase the risk of breast cancer in the
Women's Health Initiative clinical trials program
colorectal normal or cancer epithelium does not coexpress ERα and ERβ
ERβ expression resulted in the inhibition of proliferation and G1 phase cell-cycle arrest
ERβ
expression strongly inhibited cMyc and tumor growth in a xenograft mouse model
induced ERβ in CRC
cells has an antiproliferative, tumor-suppressive function that is independent of ERα
ERs also have the ability to bind many other compounds with an estrogen-like structure, including phytoestrogens
and xenoestrogens (or endocrine disruptors)
Phytoestrogens are a diverse class of natural compounds with structural similarity to estradiol
Barone et al. recently found that two ERβ-selective
phytoestrogens effectively counteracted CRC tumorigenesis and surprisingly increased ERβ expression in mice with mutations
of the tumor-suppressor gene adenomatous polyposis coli
We can conclude that estrogens are important in protecting against CRC initiation and progression, and that the protective
effect most likely is mediated by ERβ