黄芩素对人口腔鳞癌细胞增殖和侵袭的作用及其机制

目的：研究黄芩素（BAI）抑制口腔鳞癌细胞（TCA8113）增殖与侵袭及与ERK-FAK的可能关系。方法：本研究分为两次实验，每次实验有4个组：control，20 μmol/L BAI，40 μmol/L BAI，80 μmol/L BAI；control，40 μmol/L BAI，MEK抑制剂（0.33 nmol/L），MEK抑制剂（0.33 nmol/L）+40 μmol/L BAI。每组3个复孔，各组分别处理24 h和48 h。利用CCK8实验检测黄芩素对口腔鳞癌细胞的增殖抑制作用；半定量PCR及Western blot分析黄芩素对E-cadherin和Vimentin的影响；利用Western blot分析黄芩素对ERK，p-ERK，FAK以及p-FAK的调节作用；采用MEK抑制剂（U0126），利用Western blot分析其对黄芩素的调控作用。结果：黄芩苷处理组的细胞增殖率明显低于对照组（P<0.01）；黄芩素处理组对E-cadherin的mRNA和蛋白水平的上调作用明显高于对照组，对Vimentin的mRNA和蛋白水平的下调作用也明显低于对照组（P<0.01）；黄芩素处理组的p-ERK和p-FAK的蛋白水平明显低于对照组（P<0.01），但总的ERK与FAK的蛋白水平与对照组相比没有明显的差别（P<0.05）；MEK抑制剂处理组的E-cadherin的蛋白水平明显高于对照组（P<0.01），Vimentin，p-ERK和p-FAK的蛋白水平明显低于对照组（P<0.01），但总的ERK与FAK的蛋白水平与对照组相比没有明显的差别（P<0.05）。结论：黄芩素能够抑制口腔鳞癌细胞的增殖以及侵袭，其机制可能与黄芩素抑制ERK-FAK信号通路有关。

Baicalein inhibits the proliferation and invasion of oral squamous cell carcinoma and its possible signaling pathway

Objective: To investigate the relationship between the anti-proliferation effect of baicalein and extracellular signal-regulated kinase and focal adhesion kinase(ERK-FAK) signal pathway in oral squamous cell carcinoma (OSCC).Methods: The study included two parts and each part contained 4 groups, including control, 20 μmol/L BAI, 40 μmol/L BAI, 80 μmol/L BAI or control, 40 μmol/L BAI, MEK inhibitor(0.33 nmol/L),MEK inhibitor(0.33 nmol/L)+40 μmol/L BAI.Each group was treated in triplicate for 24 hours and 48 hours.Cell counting kit-8 (CCK8) was used to detect the inhibitory effect of baicalein; Polymerase chain reaction(PCR) and Western blot were used to analysis the effect of Baicalein on E-cadherin and Vimentin. The expressions of extracellular signal-regulated kinase(ERK), phosphorylated (p-ERK), focal adhesion kinase (FAK) and phosphorylated focal adhesion kinase(p-FAK) were detected by Western blot. The regulatory effect of MEK inhibitor(U0126) on Baicalein was tested by Western blot assay.Results: The survival rate of cells treated with BAI is much lower than that of control group(P<0.01); the mRNA and protein levels of E-cadherin were obviously higher than those of control group, while the mRNA and protein levels of Vimentin were lower than those of control group(P<0.01).The protein levels of p-ERK and p-FAK treated with BAI were much lower than those of control group(P<0.01), but the total ERK and FAK had no obvious changes (P<0.05).The protein level of E-cadherin treated with MEK inhibitor was higher than that of control group(P<0.01) and the protein levels of Vimentin, p-ERK and p-FAK were lower than those of control group (P<0.01), while the total protein levels of ERK and FAK were the same(P<0.05).Conclusion: Baicalein can inhibit the proliferation and invasiveness of OSCC, which may be mediated by ERK-FAK signal pathway.