BMB Rep. 2014; 47(2): 104-109  
Adenovirus vector-mediated FAM176A overexpression induces cell death in human H1299 non-small cell lung cancer cells
Hong Xie1, Jia Hu1,2, Huan Pan2, Yaxin Lou2,3, Ping Lv1,2 & Yingyu Chen1,2,*
1Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, 2Peking University Center for Human Disease Genomics, 3Proteomics Laboratory, Medical and Healthy Analytical Center, Peking University, Beijing 100191, China
Correspondence to: Tel: +86-1082802846-420; Fax: +86-1082801149; E-mail: yingyu_chen@bjmu.edu.cn
Received: April 22, 2013; Revised: May 12, 2013; Accepted: June 25, 2013; Published online: February 28, 2014.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

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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