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中国应用生理学杂志 ›› 2018, Vol. 34 ›› Issue (6): 536-540.doi: 10.12047/j.cjap.5682.2018.119

• 研究论文 • 上一篇    下一篇

黄芩素对人口腔鳞癌细胞增殖和侵袭的作用及其机制

王根桃1, 黄松2   

  1. 1. 福建省肿瘤医院口腔科, 福州 350014;
    2. 华中科技大学同济医学院附属梨园医院骨外科, 湖北 武汉 430077
  • 收稿日期:2018-02-06 修回日期:2018-10-30 出版日期:2018-11-28 发布日期:2019-03-09
  • 通讯作者: 黄松 E-mail:18510131012@sina.cn
  • 基金资助:
    华中科技大学自主创新基金项目(2015QN031)

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

WANG Gen-tao1, HUANG Song2   

  1. 1. Department of Stomatology of Fujian Tumor Hospital, Fuzhou 350014;
    2. Department of Bone Surgery, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430077, China
  • Received:2018-02-06 Revised:2018-10-30 Online:2018-11-28 Published:2019-03-09
  • Supported by:
    华中科技大学自主创新基金项目(2015QN031)

摘要: 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。

关键词: 黄芩素, 人口腔鳞癌细胞, 侵袭, 增殖, ERK-FAK

Abstract: 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.

Key words: Baicalein, human oral squamous cell carcinoma, invasiveness, proliferation, ERK-FAK

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