ABSTRACT
AIM:To investigate the molecular mechanism of wogonin on the growth and invasion of oral squa -mous-cell carcinoma (OSCC) cell line SCC-4.METHODS:After treatment with various doses (0, 20, 40, 60, 80 and 100 mg/L) of wogonin for the indicated time , MTT assay was used to evaluate cell viability .The cell apoptosis was detec-ted by flow cytometry with Annexin V and propidium iodide (Annexin V/PI) double staining.The cell invasion ability was analyzed by Transwell assay .The activation of Wnt/β-catenin signaling molecules was assessed by Western blot .RE-SULTS:Wogonin inhibited the viability and invasion of SCC-4 cells but promoted cell apoptosis in a dose-and time-de-pendent manner .Wogonin treatment obviously decreased the activation of β-catenin.Moreover, the expression of down-stream targets cyclin D1, matrix metalloproteinase-2 (MMP-2) and MMP-9 were obviously down-regulated, accompanied by the up-regulation of anti-apoptotic protein Bcl-2.Wnt/β-catenin activator LiCl remarkably attenuated the inhibitory effect of wogonin on the activation of Wnt/β-catenin signaling molecules .Importantly, the inhibition of cell growth and in-vasion ability by wogonin treatment was dramatically attenuated after LiCl exposure .CONCLUSION: Wogonin blocks SCC-4 cell growth and invasion mainly by regulating Wnt/β-catenin signaling , indicating that it is a potential suppressor for OSCC and may be a potential target for the development of anti-OSCC therapy .
ABSTRACT
AIM:To investigate the molecular mechanism of wogonin on the growth and invasion of oral squa -mous-cell carcinoma (OSCC) cell line SCC-4.METHODS:After treatment with various doses (0, 20, 40, 60, 80 and 100 mg/L) of wogonin for the indicated time , MTT assay was used to evaluate cell viability .The cell apoptosis was detec-ted by flow cytometry with Annexin V and propidium iodide (Annexin V/PI) double staining.The cell invasion ability was analyzed by Transwell assay .The activation of Wnt/β-catenin signaling molecules was assessed by Western blot .RE-SULTS:Wogonin inhibited the viability and invasion of SCC-4 cells but promoted cell apoptosis in a dose-and time-de-pendent manner .Wogonin treatment obviously decreased the activation of β-catenin.Moreover, the expression of down-stream targets cyclin D1, matrix metalloproteinase-2 (MMP-2) and MMP-9 were obviously down-regulated, accompanied by the up-regulation of anti-apoptotic protein Bcl-2.Wnt/β-catenin activator LiCl remarkably attenuated the inhibitory effect of wogonin on the activation of Wnt/β-catenin signaling molecules .Importantly, the inhibition of cell growth and in-vasion ability by wogonin treatment was dramatically attenuated after LiCl exposure .CONCLUSION: Wogonin blocks SCC-4 cell growth and invasion mainly by regulating Wnt/β-catenin signaling , indicating that it is a potential suppressor for OSCC and may be a potential target for the development of anti-OSCC therapy .