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目的研究原癌基因人类表皮生长因子受体2(HER-2)在胰腺癌演进过程中的作用,并阐明其分子机制。方法构建HER-2干扰质粒转染入PANC-1细胞。应用荧光定量PCR和Western blot检测空白组、阴性对照组和干扰组中目的基因和蛋白的表达,细胞增殖实验(CCK8)法和流式细胞术检测转染后PANC-1细胞的增殖能力和细胞周期的变化。结果与空白组和阴性对照组比较,干扰组目的蛋白和基因表达均降低(P<0.05),干扰组PANC-1细胞的增殖能力减弱,细胞周期被阻滞在G2期且凋亡增加(P<0.05)。结论 HER-2可能通过雷帕霉素靶蛋白-脂肪酸合酶(mTOR-FASN)信号通路的活性以及内源性脂肪酸代谢调节胰腺癌细胞的恶性表型。
Objective To study the role of proto-oncogene human epidermal growth factor receptor 2 (HER-2) in the progression of pancreatic cancer and elucidate its molecular mechanism. Methods The HER-2 interference plasmid was constructed and transfected into PANC-1 cells. Fluorescent quantitative PCR and Western blot were used to detect the expression of target gene and protein in blank control group, negative control group and interference group. Cell proliferation assay (CCK8) and flow cytometry were used to detect the proliferation of transfected PANC-1 cells and cells Cycle changes. Results Compared with the blank group and the negative control group, the expression of the target protein and gene in the interference group was decreased (P <0.05), the proliferation ability of PANC-1 cells in the interference group was weakened, the cell cycle was arrested in G2 phase and the apoptosis increased <0.05). Conclusion HER-2 may regulate the malignant phenotype of pancreatic cancer cells through the activity of rapamycin target protein-fatty acid synthase (mTOR-FASN) signaling pathway and endogenous fatty acid metabolism.