7,8-Dihydroxy Flavone Induces Apoptosis via Upregulation of Caspase-3 in Human Hepatocarcinoma Cell.

Abstract

Objective: 7,8-Dihydroxyflavone, a tyrosine kinase receptor agonist, is a flavonoid that has recently gained the attention of researchers due to its anticancer properties. Nevertheless, molecular pathways of 7,8-dihydroxyflavone for hepatocarcinoma are uncertain. Our aim was to identify the impact of 7,8-dihydroxyflavone on human hepatocarcinoma.

Material and methods: Human hepatocarcinoma cell line-7 cells were used as human hepatocarcinoma cells, and 7,8-dihydroxyflavone was applied to the cells at various doses. The cytotoxic and apoptotic effects of 7,8-dihydroxyflavone were determined with Alamar Blue and flow cytometry. The properties of 7,8-dihydroxyflavone on the mRNA expressions related with Bcl-2, Bax, cleaved-caspase-3 genes, and protein expressions were determined via quantitative real-time polymerase chain reaction and western blot analysis, respectively.

Results: 7,8-Dihydroxyflavone-enhanced cell death in human hepatocarcinoma cell line-7 via the overexpression of cleaved-caspase-3 (P=.003) and decreased Bcl-2 (P=.038) protein levels. Furthermore, cleavedcaspase-3 mRNA overexpression (P=.001) markedly led to 7,8-dihydroxyflavone-induced apoptosis.

Conclusion: 7,8-Dihydroxyflavone could promote apoptotic cell death by modulating caspase pathways and suppressing antiapoptotic protein. These characteristics may mediate to clinical practice of 7,8-dihydroxyflavone for prevention and therapy of hepatocarcinoma.