title: E2F1-Mediated Induction of NFYB Attenuates Apoptosis via Joint Regulation of a Pro-Survival Transcriptional Program.
abstract: The E2F1 transcription factor regulates cell proliferation and apoptosis through the control of a considerable variety of target genes. Previous work has detailed the role of other transcription factors in mediating the specificity of E2F function. Here we identify the NF-YB transcription factor as a novel direct E2F1 target. Genome-wide expression analysis of the effects of NFYB knockdown on E2F1-mediated transcription identified a large group of genes that are co-regulated by E2F1 and NFYB. We also provide evidence that knockdown of NFYB enhances E2F1-induced apoptosis, suggesting a pro-survival function of the NFYB/E2F1 joint transcriptional program. Bioinformatic analysis suggests that deregulation of these NFY-dependent E2F1 target genes might play a role in sarcomagenesis as well as drug resistance.
authors.affiliation: Duke Center for Genomic and Computational Biology, Duke University, Durham, North Carolina, United States of America; Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina, United States of America.
authors.forename: Xiaolei
authors.initials: X
authors.lastname: Jiang
authors.affiliation: Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina, United States of America.
authors.forename: Joseph Roy
authors.initials: JR
authors.lastname: Nevins
authors.affiliation: Duke Center for Genomic and Computational Biology, Duke University, Durham, North Carolina, United States of America; Department of Biomedical Engineering, Duke University Medical Center, Durham, North Carolina, United States of America.
authors.forename: Igor
authors.initials: I
authors.lastname: Shats
authors.affiliation: Duke Center for Genomic and Computational Biology, Duke University, Durham, North Carolina, United States of America; Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina, United States of America.
authors.forename: Jen-Tsan
authors.initials: JT
authors.lastname: Chi
mesh_terms: D017209:Apoptosis / Q000235:genetics; D023081:CCAAT-Binding Factor / Q000235:genetics* / Q000378:metabolism; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000235:genetics; D019008:Drug Resistance, Neoplasm / Q000235:genetics; D050687:E2F1 Transcription Factor / Q000378:metabolism*; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D012509:Sarcoma / Q000235:genetics; D014158:Transcription, Genetic; D015533:Transcriptional Activation / Q000235:genetics; D015854:Up-Regulation / Q000235:genetics
chemical_list: D023081:CCAAT-Binding Factor; D050687:E2F1 Transcription Factor; C492063:NFYB protein, human