摘要
目的研究荜拔酰胺对胃癌BGC-823细胞的抑制作用和对p53表达的调节作用及相关的分子机制。方法采用不同浓度的荜拔酰胺(0μM、2μM和20μM)对胃癌BGC-823细胞进行干预。在不同时间点(0h、24h和48h)采用MTT法对BGC-823细胞活性进行检测。干预48h后,采用qPCR对荜拔酰胺干预的BGC-823细胞p53mRNA表达水平进行检测。采用western blot对荜拔酰胺干预的BGC-823细胞p53蛋白表达水平以及PI3K和Akt活化水平进行检测。结果采用不同浓度荜拔酰胺(0μM、2μM和20μM)对胃癌BGC-823细胞进行干预后,细胞活性呈时间依赖性和浓度依赖性下降,差异均有统计学意义(P<0.05)。荜拔酰胺干预48h后,胃癌BGC-823细胞p53mRNA和蛋白的表达水平呈浓度依赖性增加而PI3K和Akt活化水平呈浓度依赖性降低,差异均存在统计学意义(P<0.05)。结论研究结果表明,荜拔酰胺可以通过下调PI3K/Akt信号通路的活化水平对胃癌BGC-823细胞的增殖产生显著抑制作用,并发现该机制与促进抑癌基因p53的表达密切相关。
To explore the anti-cancer property of piperlongumine （PL） in gastric cancer BGC-823 cells and its underlying molecular mechanism. Methods Three specific concentrations （0μM, 2μM and 20μM） of PL were included in current study. At different time points （0h, 24h and 48h）, the cell viahilities of gastric cancer BGC-823 cells were calculated by MTT assay. Meanwhile, the mRNA expression of p53 was measured by qPCR. Then, Western blot was performed to analyze the protein expression of p53 and the phosphorylation of PI3K and Akt. Results Gastric cancer BGC- 823 cells viabilities were dosage-dependently and time-dependently inhibited by PL. Meanwhile, after 48 hours of administrations, our data figured out that p53 expression was dosage-dependently up-regulated and the phosphorylation of PI3K and Akt were dosage-dependently reduced by PL in gastric cancer BGC-823 cells. Conclusion The anti-tumor property of piperlongumine （PL） very likely results from up-regulation of p53 through the inactivation of PI3K/Akt signal pathway in gastric cancer BGC-823 cells, provides the promising of the clinic use of piperlongumine in the treatment of gastric cancer and other malignant tumors in future.
出处
《西部医学》
2016年第10期1345-1348,共4页
Medical Journal of West China
基金
中国博士后科研基金(2014M552369)
