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

被引:0
作者
Abusoglu, Gulsum [1 ]
Durmus, Mukaddes Irem [2 ]
Karakurt, Serdar [2 ]
机构
[1] Selcuk Univ, Med Serv & Tech Inst, Dept Med Lab Tech, Vocat Sch Hlth Sci, Konya, Turkiye
[2] Selcuk Univ, Fac Sci, Dept Biochem, Konya, Turkiye
关键词
7; 8-DHF; apoptosis; Bax; Bcl-2; cleaved-caspase-3; HUH-7; cells; ANTIOXIDANT ACTIVITY; DOWN-REGULATION; CANCER; EXPRESSION; INDUCTION; PROTEINS; STRESS; ARREST; BCL-2; ACID;
D O I
10.5152/eurasianjmed.2023.22283
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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-dihy-droxyflavone 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-dihy-droxyflavone 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-D ihydr oxyfl avone -enha nced cell death in human hepatocarcinoma cell line-7 via the overexpres-sion of cleaved-caspase-3 (P = .003) and decreased Bcl-2 (P = .038) protein levels. Furthermore, cleaved-caspase-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-dihydroxyfla-vone for prevention and therapy of hepatocarcinoma.
引用
收藏
页码:199 / 203
页数:99
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