Adenovirus vector-mediated FAM176A overexpression induces cell death in human H1299 non-small cell lung cancer cells

被引:40
作者
Xie, Hong [1 ]
Hu, Jia [1 ,2 ]
Pan, Huan [2 ]
Lou, Yaxin [2 ,3 ]
Lv, Ping [1 ,2 ]
Chen, Yingyu [1 ,2 ]
机构
[1] Peking Univ, Hlth Sci Ctr, Minist Hlth, Key Lab Med Immunol, Beijing 100191, Peoples R China
[2] Peking Univ, Hlth Sci Ctr, Ctr Human Dis Genom, Beijing 100191, Peoples R China
[3] Peking Univ, Hlth Sci Ctr, Med & Hlth Analyt Ctr, Prote Lab, Beijing 100191, Peoples R China
基金
中国国家自然科学基金; 美国国家科学基金会;
关键词
Anti-tumor activity; Apoptosis; Autophagy; Cell cycle; FAM176A; TRANSMEMBRANE PROTEIN; EXPRESSION; P53; APOPTOSIS; AUTOPHAGY; TMEM166; CARCINOMA; CHINA;
D O I
10.5483/BMBRep.2014.47.2.090
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
FAM176A (family with sequence similarity 176 member A) is a novel molecule related to programmed cell death. A decreased expression of FAM176A has been found in several types of human tumors in including lung cancers. In the present study, we investigated the biological activities of FAM176A on the human non-small cell lung cancer cell line H1299 cells. We constructed a recombinant adenovirus 5-FAM176A vector (Ad5-FAM176A) and evaluated the expression and anti-tumor activities in vitro. Cell viability analysis revealed that the adenovirus-mediated increase of FAM176A inhibited the growth of the tumor cells in a dose-and time-dependent manner. This inhibitory effect was mediated by both autophagy and apoptosis that involved caspase activation. In addition, cell cycle analysis suggested that Ad5-FAM176A could induce cell cycle arrest at the G2/M phase, all of which suggested that adenovirus-mediated FAM176A gene transfer might present a new therapeutic approach for lung cancer treatment.
引用
收藏
页码:104 / 109
页数:6
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