Objective To investigate the mechanism and effect of signal transduction and signal transducer and activator of transcription 3(STAT3)inhibitor naphthoprofen hydrochloride(stattic)on the proliferation and apoptosis of mouse colon cancer CT26 cells.Methods Mouse colon cancer CT26 cells were treated with control group stattic solution of 0,1,5,and 10 μmol/L.Cell viability,proliferation,migration,invasion,cycle and apoptosis were investigated by CCK-8 assay,cell clonogenesis assay,cell scratch assay,Transwell assay and flow cytometry.The effect of stattic on phosphorylated STAT3(p-STAT3)expression in mouse colon cancer cells was detected by Western blot.Real-time fluorescence quantitative PCR(RT-qPCR)was used to detect the expression of B lymphoblastoma-2(Bcl-2)and human transmembrane receptor Notch-1(Notch-1)in CT26 cells after stattic treatment.Results Compared with the 0 μmol/L control group,the viability and proliferation of CT26 cells of static solution group decreased(P＜0.001),the migration and invasion rate decreased(P＜0.001),and the apoptosis rate increased with the increase of CT26 concentration(P＜0.000 1).stattic could block the cell cycle of CT26 in G1 phase,thus preventing the proliferation of CT26 cells.Western blot results showed that stattic inhibited the expression of p-STAT3 in CT26 cells(P＜0.05).The results of RT-qPCR showed that stattic down-regulated the expression of Bcl-2 and Notch1 in CT26 cells(P＜0.05).Conclusion stattic inhibited the expression of p-STAT3 protein and down-regulated expression of down-stream anti-apoptotic Bcl-2 and Notch1 signaling molecules by blocking STAT3 signal,thus inhibiting the proliferation of CT26 cells and promoting cell apoptosis.
维普
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