血管能抑素诱导甲状腺癌细胞SW579凋亡和衰老及其机制  

Canstatin induces apoptosis and senescence in SW579 cells and its mechanisms

作　　者：王传疆[1] 王雷[1] 胡海地[1] 

机构地区：[1]中国医科大学附属第一医院血管甲状腺外科,辽宁沈阳110001

出　　处：《现代肿瘤医学》2014年第6期1258-1260,共3页Journal of Modern Oncology

基　　金：国家自然科学基金资助项目(编号:81000136)

摘　　要：目的:检测血管能抑素(canstatin)对甲状腺癌SW579细胞的增殖抑制、诱导凋亡与衰老作用及其机制。方法:利用软琼脂克隆形成实验检测细胞增殖。分别利用Annexin V-FITC/PI双染和β-半乳糖苷酶染色检测细胞凋亡和衰老。Western blot技术检测可能的机制。结果:Canstatin可以明显抑制SW579细胞增殖,诱导其凋亡和衰老。处理后细胞的p-AKT蛋白水平明显下降。而caspase 3和9蛋白水平升高。结论:Canstatin通过抑制p-AKT导致SW579细胞凋亡和衰老。Objective：To detect the effects and mechanisms of canstatin on thyroid cancer cell SW579. Methods：The proliferative ratio of SW579 cells after treated with canstatin was detected by soft agarose assay. Annexin-V/FITC and PI double -staining and SA -β -gal staining were used to detect the apoptosis and the senescence of SW579 cells after treated with canstatin,respectively. The possible mechanisms were analyzed by Western-blot. Re-sults：Canstatin could inhibit the proliferation and induce apoptosis and senescence in SW579 cells. The level of p-AKT was lower in treated cells than untreated ones. The levels of caspase 3 and 9 expression were up-regulated in SW579 cells by canstatin. Conclusion：Canstatin could induce apoptosis and senescence in SW579 cells by suppress-ing p-AKT.

关 键 词：SW579细胞 CANSTATIN 凋亡 衰老 p-AKT 

分 类 号：R730[医药卫生—肿瘤] R736.1[医药卫生—临床医学]