Aesculus pavia foliar saponins: defensive role against the leafminer Cameraria ohridella.

The effects of phytoestrogens have been studied in the hypothalamic-pituitary-gonadal axis and in various non-gonadal targets. Epidemiologic and experimental evidence indicates a protective effect of phytoestrogens also in colorectal cancer. The mechanism through which estrogenic molecules control colorectal cancer tumorigenesis could possibly involve estrogen receptor β, the predominantly expressed estrogen receptor subtype in colon mucosa. To validate this hypothesis, we therefore used an engineered human colon cancer cell line induced to overexpress estrogen receptor β, beside its native cell line, expressing very low levels of ERβ and not expressing ERα; as a phytoestrogenic molecule, we used kaempferide triglycoside, a glycosylated fl avonol from a Dianthus caryophyllus cultivar. The inhibitory properties of this molecule toward vegetal cell growth have been previously demonstrated: however, no data on its activity on animal cell or information about the mechanism of this activity are available. Kaempferide triglycoside proved to inhibit the proliferation of native and estrogen receptor β overexpressing colon cancer cells through a mechanism not mediated by ligand binding dependent estrogen receptor activation. It affected HCT8 cell cycle progression by increasing the G0/G1 cell fraction and in estrogen receptor β overexpressing cells increased two antioxidant enzymes. Interestingly, the biological effects of this kaempferide triglycoside were strengthened by the presence of high levels of estrogen receptor β. Pleiotropic molecular effects of phytoestrogens may explain their protective activity against colorectal cancer and may represent an interesting area for future investigation with potential clinical applications