title: Adenovirus vector-mediated FAM176A overexpression induces cell death in human H1299 non-small cell lung cancer cells.
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.
authors.affiliation: Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Beijing 100191, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Xie
authors.affiliation: Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Beijing 100191, China; Peking University Center for Human Disease Genomics, Peking University, Beijing 100191, China.
authors.forename: Jia
authors.initials: J
authors.lastname: Hu
authors.affiliation: Peking University Center for Human Disease Genomics, Peking University, Beijing 100191, China.
authors.forename: Huan
authors.initials: H
authors.lastname: Pan
authors.affiliation: Peking University Center for Human Disease Genomics, Peking University, Beijing 100191, China; Proteomics Laboratory, Medical and Healthy Analytical Center, Peking University, Beijing 100191, China.
authors.forename: Yaxin
authors.initials: Y
authors.lastname: Lou
authors.affiliation: Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Beijing 100191, China; Peking University Center for Human Disease Genomics, Peking University, Beijing 100191, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Lv
authors.affiliation: Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Beijing 100191, China; Peking University Center for Human Disease Genomics, Peking University, Beijing 100191, China.
authors.forename: Yingyu
authors.initials: Y
authors.lastname: Chen
mesh_terms: D000256:Adenoviridae / Q000235:genetics*; D017209:Apoptosis; D001343:Autophagy; D002289:Carcinoma, Non-Small-Cell Lung / Q000378:metabolism / Q000473:pathology; D053148:Caspase 3 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D045744:Cell Line, Tumor; D059565:G2 Phase Cell Cycle Checkpoints; D005822:Genetic Vectors / Q000378:metabolism; D006801:Humans; D008175:Lung Neoplasms / Q000378:metabolism / Q000473:pathology; D059566:M Phase Cell Cycle Checkpoints; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D011994:Recombinant Proteins / Q000096:biosynthesis / Q000235:genetics
chemical_list: C524094:EVA1A protein, human; D008565:Membrane Proteins; D011994:Recombinant Proteins; D053148:Caspase 3; D053453:Caspase 9