HOMOERIODICTYOL INHIBITS SURVIVAL AND MIGRATION OF ANDROGEN-RESISTANT PROSTATE CANCER CELLS IN VITRO.

Flavonoids, naturally occurring compounds found in plant-based products, are being investigated as potential non-invasive treatments due to their ability to inhibit cell growth, induce apoptosis, and prevent cell migration. This study aims to investigate the effects of homoeriodictyol, a member of the flavanone group, both alone and in combination with docetaxel on the survival, apoptosis, migration, and proliferation of prostate cancer cells. Androgen-resistant prostate cancer PC3 cells were treated with various concentrations of homoeriodictyol, docetaxel, or a combination of both for 72 h. The treatment effects on cell survival, migration, apoptosis, and gene expression were evaluated using the MTT test, wound healing assay, Hoechst staining, and realtime PCR. Homoeriodictyol induced apoptosis in PC3 cells in a concentration-dependent manner, with a more potent effect in combination with docetaxel. Apoptosis occurred through both intrinsic and extrinsic caspase pathways, leading to the upregulation of CASP3, CASP8, TP53, BAX, and CYCS, and downregulation of BCL2 mRNA expression. Homoeriodictyol also exhibited antimigratory effects via upregulating CDH1, while decreasing CDH2 expression levels. It suppressed epithelial-mesenchymal transition by downregulating the expression of TWIST, SNAIL, and ZEB1, which correlated with the observed antimigratory effects in wound healing assays. Homoeriodictyol exerted potent effects and inhibited prostate cancer cell proliferation and migration, especially when used in combination with docetaxel.