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作 者:杨清滔[1] 谷江[2] 石家齐[1] 贾本忠[1] 顾昌世[1] 张永春[2] 朱致晖 姚茂良 刘淼[2] 夏剑锋[2]
机构地区:[1]贵州医科大学附属白云医院,贵州贵阳550004 [2]贵州医科大学附属医院,贵州贵阳550004 [3]贵州省妇幼保健院,贵州贵阳550000
出 处:《贵阳医学院学报》2015年第10期1043-1046,1050,共5页Journal of Guiyang Medical College
基 金:贵州省科技厅社会攻关计划项目[黔科合sy字(2011)3060]
摘 要:目的:研究斯钙素1(stanniocalcin1,STC-1)对肾癌细胞生长的调控机制。方法:体外培养肾癌细胞,用0、0.1、0.5和1.0 nmol/L STC-1溶液浸染肾癌细胞,分别为对照组、低剂量组、中剂量组和高剂量组;分别用MTT法检测各组肾癌细胞的增殖情况,RT-PCR及ELISA法检测各组肾癌细胞中缺氧诱导因子1α(HIF-1α)、STC-1基因及蛋白的表达,荧光分光光度计检测各组细胞内Ca2+水平。结果:随着STC-1蛋白给药浓度的增加,细胞内HIF-1α、STC-1的表达及Ca2+水平逐渐下降,细胞的促增殖作用逐渐降低,在低剂量组出现一过性增加。结论:STC-1蛋白可能通过调节HIF-1α、Ca2+的水平,促进肾癌细胞增殖,而该促增殖作用可能会因为STC-1对HIF-1α的抑制而逐渐减弱,从而调控肾癌细胞的生长平衡。Objective: To research the regulation machenism of Stanniocalcinl (STC-1) on renal carcinoma cells. Methods: Renal carcinoma cells were cultured in vitro, and STC-1 solutions of different concentration were added to the culture medium. According to the different concentration, re- nal carcinoma cells were divided into control group, low-dose group (0.1 nmol/L STC-1 ), middle- dose group (0.5 nmol/L STC-I ), high-dose group ( 1.0 nmol/L STC-1 ). The proliferation of cells, expressions of HIF-1 ot, STC-1 and levels of Ca^2+ were detected by MTT, RT-PCR, ELISA and Fluo- rescence Spectrophotometer respectively. Results: The results showed that the cells treated with STC-1 protein exhibited characteristics of proliferation. And along with the increase of STC-1 protein concen- tration, the proliferation of cells, expressions of HIF-lot and STC-1, levels of Ca^2+ were down-regula- ted. And a transient increase of proliferation of cells occurred in the low-dose group. Conclusions: STC-I protein may participate in malignant proliferation of renal carcinoma cells through depressing HIF-1 ot or down-regulation CaR + , which could wear off when HIF-1 α is inhibited by redundant STC-1, thus regulate the growth balance of renal carcinoma cells.
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