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目的为解释新发糖尿病合并胰腺癌预后差的现象,本研究拟探讨胰岛素影响胰腺癌细胞钠代谢的分子机制。方法在高糖DMEM中培养胰腺癌细胞SW1990,用不同浓度胰岛素刺激细胞,在不同时间检测培养上清中Na+浓度,分析Na+随胰岛素浓度和时间变化的规律。同时检测胰岛素对血清和糖皮质激素诱导的蛋白激酶1(SGK1)的影响,并分析其中的信号通路。结果胰岛素刺激SW1990细胞后,培养上清中Na+浓度下降(P<0.05),SGK1蛋白表达量增加(P<0.05),且Na+浓度的下降幅度与SGK1蛋白水平相关(r=0.715,P<0.01);胰岛素处理后乙酰化修饰关键基因CREBBP和EP300表达明显上调(P<0.05)。结论胰岛素可促进胰腺癌细胞吸收钠离子,与SGK1基因的表达水平相关,其中乙酰化修饰可能发挥一定作用。
Objective To explain the poor prognosis of newly diagnosed diabetes mellitus combined with pancreatic cancer, this study was to explore the molecular mechanism of insulin on the sodium metabolism of pancreatic cancer cells. Methods Pancreatic cancer cell line SW1990 was cultured in high glucose DMEM, and the cells were stimulated with different concentrations of insulin. Na + concentration in culture supernatant was detected at different times, and the regularity of Na + with insulin concentration and time was analyzed. At the same time, the effects of insulin on serum and glucocorticoid-induced protein kinase 1 (SGK1) were assayed and their signal pathways analyzed. Results After SW1990 cells were stimulated with insulin, the concentration of Na + in culture supernatant decreased (P <0.05) and the expression of SGK1 protein increased (P <0.05), and the decrease of Na + concentration was correlated with SGK1 protein level (r = 0.715, ). The expressions of CREBBP and EP300, the key genes for acetylation modification after insulin treatment, were significantly up-regulated (P <0.05). Conclusion Insulin can promote pancreatic cancer cells to absorb sodium ion, which is related to the expression level of SGK1 gene. Among them, acetylation may play a role.