ArticleThe EMBO journal1994
The E6/E7 promoter of extrachromosomal HPV16 DNA in cervical cancers escapes from cellular repression by mutation of target sequences for YY1.
Article in The EMBO journal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 162 citations in OpenAlex.
- Human papillomavirus 16 non-European variants are preferentially associated with high-grade cervical lesions.PloS one · 2014Trial
- Assessing the dynamics and macromolecular interactions of the intrinsically disordered protein YY1.Bioscience reports · 2023Article
- Extrachromosomal Amplification of Human Papillomavirus Episomes Is a Mechanism of Cervical Carcinogenesis.Cancer research · 2023Article
- Characterization of Human Papillomavirus 16 from Kinshasa (Democratic Republic of the Congo)-Implications for Pathogenicity and Vaccine Effectiveness.Microorganisms · 2022Article
- Dual Role of YY1 in HPV Life Cycle and Cervical Cancer Development.International journal of molecular sciences · 2022Review
- Effect of the transcription factor YY1 on the development of pancreatic endocrine and exocrine tumors: a narrative review.Cell & bioscience · 2021Review
- Oncogenic HPV promotes the expression of the long noncoding RNA lnc-FANCI-2 through E7 and YY1.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Molecular mechanisms of HPV mediated neoplastic progression.Infectious agents and cancer · 2016Review
- Function of YY1 in Long-Distance DNA Interactions.Frontiers in immunology · 2014Review
- Article
- Genomic differences in the background of different severity in juvenile-onset respiratory papillomatoses associated with human papillomavirus type 11.Medical microbiology and immunology · 2013Article
- A point mutation in the DNA-binding domain of HPV-2 E2 protein increases its DNA-binding capacity and reverses its transcriptional regulatory activity on the viral early promoter.BMC molecular biology · 2012Article
- Primary human cervical carcinoma cells require human papillomavirus E6 and E7 expression for ongoing proliferation.Virology · 2012Article
- Mechanisms of Yin Yang 1 in oncogenesis: the importance of indirect effects.Critical reviews in oncogenesis · 2011Review
- In vitro progression of human papillomavirus 16 episome-associated cervical neoplasia displays fundamental similarities to integrant-associated carcinogenesis.Cancer research · 2010Article
- Upstream regulatory region alterations found in human papillomavirus type 16 (HPV-16) isolates from cervical carcinomas increase transcription, ori function, and HPV immortalization capacity in culture.Journal of virology · 2009Article
- Human papillomavirus type 16 variant analysis of E6, E7, and L1 genes and long control region in biopsy samples from cervical cancer patients in north India.Journal of clinical microbiology · 2008Article
- New HPV-16 European and non-European variants in Central Brazil.Virus genes · 2007Article
- Transcription factor YY1: structure, function, and therapeutic implications in cancer biology.Oncogene · 2006Review
- Variant upstream regulatory region sequences differentially regulate human papillomavirus type 16 DNA replication throughout the viral life cycle.Journal of virology · 2005Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human papillomavirus type 16 (HPV16) induces squamous intraepithelial lesions of the cervical mucosa which may develop into invasive cancer. The expression of viral oncogenes in advanced neoplasias appears increased relative to the proliferating cell layers of low grade lesions raising questions about molecular mechanisms of deregulation of transcription. In a lymph node metastasis of a cervical cancer, we observed full-length HPV16 plasmids and molecules with a small deletion, which was mapped to the long control region (LCR). Both wild type and shortened LCR were amplified by PCR, cloned into the promoter test plasmid pBLCAT6 and sequenced to identify a 107 bp deletion from position 7794 to 7901 in the short LCR. CAT expression in cervical cancer-derived HT3, SiHa and CaSki cells appeared 5- to 6-fold increased under the control of the short LCR. This could be traced back to elevated levels of mRNA initiated at the viral oncogene promoter. A slight further increase in CAT expression was noted in the presence of the HPV16 E2 protein which is probably due to the deletion of one E2 binding site and consequent relief from E2 repression. Computer-assisted sequence analysis and band-shift experiments with purified YY1 protein and wild type or mutated oligonucleotides identified four binding sites for this cellular transcriptional repressor within the promoter-proximal segment of the HPV16 LCR, three of which were removed by the deletion. A LCR fragment comprising these YY1 binding sites was cloned in front of the heterologous thymidine kinase gene promoter and suppressed CAT expression 3- to 4-fold.(ABSTRACT TRUNCATED AT 250 WORDS)
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