resveratrol inhibits wntsignaling by affecting β-catenin and gsk-3β gene expression in hct-116 human colorectal cancer cells

Background: colorectal cancer is one of the mostly diagnosed malignancies worldwide. the main risk factors for colorectal cancer include the mutation of tumor suppressor genes or proto-oncogenes and unhealthy lifestyle. vegetable and fruit consumption with multiple anticancer agents can reduce the risk of colon cancer. resveratrol is a natural polyphenolic product that inhibits proliferation and induces apoptosis through several pathways. in this study, the effects of resveratrol on β-catenin (ctnnb1) and gsk-3β expression, affecting the wnt-signaling pathway, were examined and morphology changes analyzed in colon cancer cells with high levels of β-catenin such as hct-116. methods: hct-116 cells were seeded into 6-well plates and the cells were treated with various concentrations of resveratrol (25, 50 and 100 μm) for 24, 48 and 72 hours respectively. quantitative real-time pcr examined β-catenin and gsk-3β expression and morphology changes were analyzed. results: our result showed that in 25 and 50 μm concentrations, resveratrol reduces β-catenin and gsk-3β expression in 24 h (p-value; 0.001). gene expressions were found to increase in 48 h and 72 h treatment with resveratrol in the concentrations of 50 and 100 μm respectively (p-value; 0.001). conclusion: considering our data, we suggest that low doses of resveratrol could reduce β-catenin expression, which can affect the wnt-signaling pathway. while high doses can increase the gsk-3β expression, playing a role in the destruction of β-catenin, inhibition of its accumulation in the cytoplasm and nuclear, apoptosis induction and cellular proliferation inhibition. on the other hand, low doses of resveratrol can decrease gsk-3β expression and suppress proliferation. abbreviations: lef/tcf, lymphoid enhancing factor/t-cell factor; apc, adenomatous polyposis coli; gsk-3β, glycogen synthase kinase 3b; ck, casein kinase 1; rsv, resveratrol; dmso, dimethyl sulfoxide; dmem-f12, dulbecco's modified eagle's medium f-12; fbs, fetal bovine serum; cin, chromosomal instability; pi3k, phosphatidylinositol- 3-kinase; tgf-β, transforming growth factor-β; gfr, growth factor receptor; kras, kirsten rat sarcoma viral oncogene homolog; pten, phosphatase and tensin homolog; cox, cytochrome c oxidase; igf-1r, insulin-like growth factor 1 (igf-1) receptor; akt, protein kinase b (pkb)