Impacts of phillygenin on proliferation,apoptosis,and epithelial mesenchymal transformation in prostate cancer by regulating Janus kinase 2/signal transduction and transcription activating factor 3 signaling pathway
Objective To investigate the impacts of phillygenin(PHI)on proliferation,apoptosis,and epithelial mesenchymal transformation in prostate cancer(PCa)and its mechanism.Methods DU-145 and LNCap-FGC cells were cultured in vitro and divided into control group,phillygenin group(PHI group),Janus kinase 2(JAK2)inhibitor group(Ag490 group),and phillygenin+activator group(PHI+Colivelin group).Cell viability,cell cloning ability,scratch healing rate,and cell invasion were detectede respectively.Immunohistochemistry was applied to analyze the expression of E-cadherin,N-cadherin and Vimentin.Western blot was applied to detect the expression of JAK2,p-JAK2,signal transduction and transcriptional activator 3(STAT3),p-STAT3 proteins.Results Compared with the control group,the cell survival rate,cell clone number,scratch healing rate,cell invasion number,N-cadherin,Vimentin,p-JAK2 and p-STAT3 expression of DU-145 and LNCap-FGC cells in the PHI group and Ag490 group were significantly decreased,the apoptosis rate and E-cadherin expression were significantly increased(P＜0.05),and there was no significant difference between PHI group and Ag490 group(P＞0.05).Compared with the PHI group,the cell survival rate,cell clone number,cell scratch healing,cell invasion number,N-cadherin,Vimentin,p-JAK2 and p-STAT3 expression in the PHI+Colivelin group were significantly increased,the apoptosis rate and E-cadherin were significantly decreased(P＜0.05).Conclusions PHI can inhibit the JAK2/STAT3 signaling pathway to inhibit the proliferation and induce apoptosis of PCa cells,and reverse the process of epithelial mesenchymal transformation of DU-145 and LNCap-FGC.
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