14-3-3σ调控p27抑制Rat1-Akt细胞增殖  

14-3-3σ regulates p27 and inhibits Rat1-Akt cell proliferation

作　　者：杨惠玲[1] 夏洪平[1] 赵睿颖[2] 夏云飞[3] 黄文林[3] LEE Mong-hong 

机构地区：[1]中山大学病理生理学教研室,广东广州510080 [2]美国德州大学M.D.Anderson癌症中心,德州77030 [3]中山大学肿瘤防治中心,广东广州510060

出　　处：《中国病理生理杂志》2007年第10期2035-2038,共4页Chinese Journal of Pathophysiology

基　　金：广东省重大科技专项基金资助项目(No.2004A30801006);广东省国际合作科技计划资助项目(No.2004B50301003);广州市国际合作资助项目(No.4205001)

摘　　要：目的:研究腺病毒介导14-3-3.σ(Ad-14-3-.3σ)对Akt过表达Rat1-Akt细胞增殖的影响,并探讨其作用是否通过调控p27而实现。方法:通过5-溴-2′脱氧尿嘧啶(B rdU)实验检测Ad-14-3-3.σ对Rat1-Akt细胞增殖的影响,并通过激酶分析法和免疫荧光实验探讨Ad-14-3-3.σ对p27磷酸化水平及其在细胞内定位的影响。结果:Ad-14-3-3σ转染的细胞B rdU阳性率(45%)低于PBS处理组(100%)或Ad-β-gal转染的对照组细胞(98%)。14-3-3σ可降低磷酸化p27的水平和减少Akt介导的p27在胞浆中的定位。结论:转染14-3-3σ基因能抑制Akt过表达细胞株Rat1-Akt增殖,14-3-3σ通过降低Akt激酶磷酸化p27的活性,阻断Akt介导的p27胞浆错位,从而发挥其抑制Rat1-Akt细胞增殖。AIM： The present study was designed to investigate the effect of adenovirus -mediated 14 -3 -3σ on the proliferation of Rat1 - Akt cells and to explore whether this effect is completed regulating p27. METHODS： The effect of Ad - 14 - 3 - 3σ gene transfection on Rat1- Akt cell proliferation was observed by using 5 - bromodeoxyuridine （BrdU）. Then immunofluorescence and kinase assay were used to detect the effect of Ad - 14 - 3 - 3or on the phosphorylated level and intracellular location of p27. RESULTS ： Ad - 14 - 3 - 3σ - infected cells had fewer BrdU - positive cells （45%） than control （ which was set at 100% ）. However, Ad - 13 - gal - infected cells had a high percentage of BrdU - positive cells （98%）. 14- 3 -3σ gene transfection downregulated phosphorylation level of p27 and decreased Akt- mediated intracellular location of p27. CONCLUSION： Transfection of 14 -3 -3σ gene suppresses the proliferation of Akt overexpession cell line Rat1- Akt. 14 -3 -3σ decreases phosphorylation of p27 by downregulating Akt kinase, blocks Akt - mediated cytoplasm dislocation of p27, and inhibits proliferation of Rat1 - Akt cells.

关 键 词：基因 14—3—3σ P27 蛋白激酶B Rat1—Akt细胞 

分 类 号：R735.905.3[医药卫生—肿瘤]