TGFBI对胃癌MGC-803细胞侵袭转移及血管生成的影响  

Effect of TGFBI on invasion,metastasis and angiogenesis of gastric cancer cell line MGC-803

作　　者：黄芳 陈晓帆 Huang Fang;Chen Xiaofan(Department of Pharmacy,Sanming First Hospital Affiliated Fujian Medical University,Sanming 365000,China;Department of Traditional Chinese Medicine,Sanming First Hospital Affiliated Fujian Medical University,Sanming 365000,China)

机构地区：[1]福建医科大学附属三明第一医院药学部,三明365000 [2]福建医科大学附属三明第一医院中医科,三明365000

出　　处：《中国组织化学与细胞化学杂志》2023年第6期539-546,共8页Chinese Journal of Histochemistry and Cytochemistry

摘　　要：目的 探讨转化生长因子β诱导物(transforming growth factor β induced, TGFBI)在胃癌中的表达及其对胃癌细胞MGC-803侵袭转移及血管生成的影响和分子机制。方法 RT-q PCR和免疫组织化学检测人胃癌组织及胃癌细胞株中TGFBI的表达。转染小干扰RNA(si-TGFBI)构建人胃癌MGC-803细胞TGFBI敲减模型,MTT实验测定细胞增殖,划痕实验及Transwell侵袭实验评估侵袭转移;Matrigel体外成管实验观察血管生成;免疫荧光及Western blot评估相关目的蛋白的表达及PI3K/AKT/mTOR信号通路的活性。结果 胃癌组织及胃癌细胞株中TGFBI的表达均显著升高。转染si-TGFBI可抑制胃癌MGC-803细胞增殖、血管生成以及侵袭转移,同时上调E-cadherin表达,并下调N-cadherin、Snail以及Vimentin的表达,抑制上皮-间充质转化进程。此外,转染si-TGFBI可显著抑制胃癌MGC-803细胞PI3K/AKT/mTOR信号通路的活性。结论 TGFBI在胃癌中高表达,高表达的TGFBI可能通过激活PI3K/AKT/mTOR信号促进胃癌细胞的增殖、侵袭转移及血管生成。Objective To investigate transforming growth factorβinduced(TGFBI)expression in gastric cancer tissues and explore its effect and mechanisms on invasion,metastasis and angiogenesis of gastric cancer cell line MGC-803.Methods The ex-pression levels of TGFBI in gastric cancer tissues and cell lines were detected with immunohistochemistry staining and quantitative real-time PCR(RT-qPCR).Small interfering RNA(si-TGFBI)was employed to construct TGFBI knockdown model in gastric cancer cell MGC-803.Then cell proliferation,migration,invasion and angiogenesis were evaluated with MTT assay,scratch test,Transwell invasion assay and in vitro Matrigel tubular formation assay,respectively.Related protein expression and activation of PI3K/AK-T/mTOR signaling pathway were assessed by immunofiuorescence and Western blot assay.Results Expression level of TGFBI was remarkably increased in gastric cancer tissues and cell lines,such as MGC-803,SGC7901 and AGS.Transfection of si-TGFBI inhibited proliferation,angiogenesis,invasion and metastasis in gastric cancer cell MGC-803.In addition,si-TGFBI up-regulated the expression of E-cadherin,while down-regulated the expression of N-cadherin,Snail and Vimentin,with inhibition of epithelial-mesenchymal tran-sition process.Furthermore,transfection of si-TGFBI suppressed the activation of PI3K/AKT/mTOR signaling pathway.Conclusion TGFBI is highly expressed in gastric cancer,and enhanced levels of TGFBI may promote the proliferation,invasion and metastasis of gastric cancer cells and angiogenesis by activating PI3K/AKT/mTOR signaling pathway.

关 键 词：转化生长因子β诱导物 胃癌 侵袭 血管生成 PI3K/AKT/mTOR信号 

分 类 号：R735.2[医药卫生—肿瘤]