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http://dx.doi.org/10.5483/BMBRep.2014.47.2.090

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

Xie, Hong (Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Peking University)
Hu, Jia (Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Peking University)
Pan, Huan (Peking University Center for Human Disease Genomics, Peking University)
Lou, Yaxin (Peking University Center for Human Disease Genomics, Peking University)
Lv, Ping (Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Peking University)
Chen, Yingyu (Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Peking University)
Publication Information
BMB Reports / v.47, no.2, 2014 , pp. 104-109 More about this Journal
Abstract
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.
Keywords
Anti-tumor activity; Apoptosis; Autophagy; Cell cycle; FAM176A;
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