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目的:初步探索STAT3与HGC27胃癌细胞增殖的关系。方法:用T4 DNA连接酶将外源片段与酶切后的p LKO.1载体连接,将构建的重组质粒转染293T细胞,48 h后收集上清用于感染HGC27细胞,Western印迹检测蛋白的表达,生长实验检测其对肿瘤细胞增殖的影响。结果:基因测序和双酶切鉴定表明敲低STAT3质粒构建成功;慢病毒质粒有效抑制HGC27细胞中STAT3蛋白水平,抑制STAT3对HGC27细胞的增殖有明显抑制作用。结论:在PTEN缺失的HGC27胃癌细胞中STAT3促进肿瘤增殖,但STAT3并不是在所有PTEN缺失的肿瘤细胞中都发挥抑制肿瘤形成的作用。
Objective: To explore the relationship between STAT3 and proliferation of gastric cancer cell line HGC27. METHODS: The exogenous DNA fragment was ligated with the pLKO.1 vector digested with T4 DNA ligase. The recombinant plasmids were transfected into 293T cells. After 48 hours, the supernatants were collected for infection of HGC27 cells. Western blotting was used to detect the protein Expression and growth assays were used to detect the effect on tumor cell proliferation. Results: The gene sequencing and restriction enzyme digestion showed that knockdown of STAT3 plasmid was successful. The lentiviral plasmid effectively inhibited the STAT3 protein level in HGC27 cells and inhibited the effect of STAT3 on the proliferation of HGC27 cells. CONCLUSIONS: STAT3 promotes tumor proliferation in PTEN-deficient HGC27 gastric cancer cells, but STAT3 does not inhibit tumor formation in all PTEN-deficient tumor cells.