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LASS2 interacts with V-ATPase and inhibits cell growth of hepatocellular carcinoma
Author(s): TANG Ning1, 2, JIN Jie3, DENG Yun2, KE Rong-Hu2, SHEN Qiu-Jin2, FAN Shao-Hua2, QIN Wen-Xin2, * 1Shanghai Medical College, Fudan University, Shanghai 200032, China, 2National Laboratory for Oncogenes and Related Genes, Shanghai Cancer Institute, Shanghai 200032, China, 3School of Life Sciences, Jiangsu University, Zhenjiang 212013, China
Pages: 196-
202
Year: 2010
Issue:
3
Journal: Acta Physiologica Sinica
Keyword: GetLinkList(KeywordFilter('人源性长寿保障基因2; 肝癌; 细胞生长; 凋亡; 细胞色素c'); 'kw'; 'CJFD');
Abstract: 人源性长寿保障基因2(Homo sapiens longevity assurance homologue2,LASS2)是本实验室克隆到的一个与酵母长寿保障基因LAG1高度同源的人类新基因。前期研究显示,LASS2可与V-ATPase质子泵的c亚基ATP6L结合,过表达LASS2可以抑制肝癌细胞SMMC-7721的生长。本研究旨在探讨LASS2对V-ATPase质子泵功能的调节是否参与LASS2对肝癌细胞生长的抑制作用。使用本室构建、保存的pCMV-HA2-LASS2质粒瞬时转染肝癌细胞(HCCLM3),而未转染质粒的HCCLM3细胞作为空白对照,运用CCK-8试剂盒检测细胞生长情况;采用BCECF-AM和BCECF氢离子敏感探针分别测定细胞内、外H+浓度;应用流式细胞仪检测细胞凋亡;Western blot检测线粒体和胞质内细胞色素c(cytochrome c,Cytc)、胞质中的无活性pro-caspase-3的表达情况。结果显示,外源性LASS2的过表达对HCCLM3细胞生长有抑制作用;过表达LASS2使HCCLM3细胞内H+浓度上升,细胞凋亡率提高,线粒体Cyt c释放增加,胞质中pro-caspase-3含量下降。以上结果提示提示LASS2可能通过调控V-ATPase质子泵的功能,提高细胞内H+浓度,从而激活细胞线粒体凋亡途径、抑制肝癌细胞的生长。
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