作者: Manli Na , Dongfeng Chen , Bo Holmqvist , Liang Ran , Jie Jin
DOI: 10.1016/J.VIROL.2014.03.025
关键词: Histone deacetylase 、 Trichostatin A 、 Tropism 、 Cancer research 、 Biology 、 BMI1 、 Murine leukemia virus 、 HEK 293 cells 、 Adenoviridae 、 Histone deacetylase activity
摘要: Polycomb ring finger oncogene BMI1 (B cell-specific Moloney murine leukemia virus integration site 1) plays a critical role in development of several types cancers. Here, we report an inverse relationship between levels expression and adenovirus (Ad) progeny production. Enforced A549 cells impaired Ad In contrast, knocking-down endogenous enhanced production conditionally replicating wild-type Ad5 Ad11p. vectors overexpressing were not the replication genomes E1A structural proteins. However, 293 infected by vector contained large proportion morphologically irregular particles. This effect was reversed pre-treated with histone deacetylase (HDAC) inhibitor trichostatin A (TSA) parallel infectious Our findings suggest inhibitory morphogenesis that can be implied tropism Ad-mediated cancer therapy.