Sulforaphane Inhibits Proliferation and Apoptosis of Colorectal Cancer Cells by Down-Regulating the Cyclooxygenase-2/Protein Kinase B/Glycogen Synthase Kinase-3 Beta Signaling Pathway
Department of Gastrointestinal Surgery, Shenzhen People's Hospital, Luohu, Shenzhen 518020, China
Mingwei Li, Department of Gastrointestinal Surgery, Shenzhen People's Hospital, Luohu, Shenzhen 518020, China, E-mail: email@example.com
To determine the effects of sulforaphane on the proliferation and apoptosis of colorectal cancer cell line HCT116 and the levels of proteins related to the cyclooxygenase-2/protein kinase B/glycogen synthase kinase-3 beta signal transduction. Colorectal cancer HCT116 cell lines were cultured in vitro and assigned into sulforaphane (30, 60 and 120 μM) groups, simple cisplatin group and cisplatin+sulforaphane group. The relative survival rate and apoptosis rate of HCT116 cells were determined by cell counting kit-8 assay and flow cytometry, respectively. Besides, the expression levels of proteins survivin, caspase-3, cyclooxygenase-2, protein kinase B, phosphorylated-protein kinase B, glycogen synthase kinase-3 beta and phosphorylated-glycogen synthase kinase-3 beta in HCT116 cells were measured through Western blotting. Compared with that in control group, the relative survival rate of cells in 60 and 120 μM sulforaphane groups, simple cisplatin group and cisplatin+sulforaphane group declined significantly (p<0.05). Sulforaphane can exert its anti-tumor effect by inducing apoptosis and suppressing proliferation of HCT116 cells and its mechanism may be associated with inhibition on the activation of the cyclooxygenase-2/protein kinase B/ glycogen synthase kinase-3 beta signaling pathway.