Linked Life Data

21821000

Source:http://linkedlifedata.com/resource/pubmed/id/21821000

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-8-29
pubmed:abstractText
Deregulation of the expression of human papillomavirus (HPV) oncogenes E6 and E7 plays a pivotal role in cervical carcinogenesis because the E6 and E7 proteins neutralize p53 and Rb tumor suppressor pathways, respectively. In approximately 90% of all cervical carcinomas, HPVs are found to be integrated into the host genome. Following integration, the core-enhancer element and P105 promoter that control expression of E6 and E7 adopt a chromatin structure that is different from that of episomal HPV, and this has been proposed to contribute to activation of E6 and E7 expression. However, the molecular basis underlying this chromatin structural change remains unknown. Previously, BAF53 has been shown to be essential for the integrity of higher-order chromatin structure and interchromosomal interactions. Here, we examined whether BAF53 is required for activated expression of E6 and E7 genes. We found that BAF53 knockdown led to suppression of expression of E6 and E7 genes from HPV integrants in cervical carcinoma cell lines HeLa and SiHa. Conversely, expression of transiently transfected HPV18-LCR-Luciferase was not suppressed by BAF53 knockdown. The level of the active histone marks H3K9Ac and H4K12Ac on the P105 promoter of integrated HPV 18 was decreased in BAF53 knockdown cells. BAF53 knockdown restored the p53-dependent signaling pathway in HeLa and SiHa cells. These results suggest that activated expression of the E6 and E7 genes of integrated HPV is dependent on BAF53-dependent higher-order chromatin structure or nuclear motor activity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1090-2104
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
26
pubmed:volume
412
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
328-33
pubmed:dateRevised
2011-11-7
pubmed:meshHeading
pubmed-meshheading:21821000-Actins, pubmed-meshheading:21821000-Chromosomal Proteins, Non-Histone, pubmed-meshheading:21821000-DNA-Binding Proteins, pubmed-meshheading:21821000-Female, pubmed-meshheading:21821000-Gene Expression Regulation, Viral, pubmed-meshheading:21821000-Gene Knockdown Techniques, pubmed-meshheading:21821000-HeLa Cells, pubmed-meshheading:21821000-Human papillomavirus 18, pubmed-meshheading:21821000-Humans, pubmed-meshheading:21821000-Oncogene Proteins, Viral, pubmed-meshheading:21821000-Promoter Regions, Genetic, pubmed-meshheading:21821000-RNA Interference, pubmed-meshheading:21821000-Transcription, Genetic, pubmed-meshheading:21821000-Transcriptional Activation, pubmed-meshheading:21821000-Tumor Suppressor Protein p53, pubmed-meshheading:21821000-Uterine Cervical Neoplasms
pubmed:year
2011
pubmed:articleTitle
Suppression of HPV E6 and E7 expression by BAF53 depletion in cervical cancer cells.
pubmed:affiliation
Department of Bioscience and Biotechnology, Hankuk University of Foreign Studies, Yongin 449-791, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't