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Title: Repression of MHC class I transcription by HPV16E7 through interaction with a putative RXR{beta} motif and NF-{kappa}B cytoplasmic sequestration

Abstract

Down-regulation of transcription of the MHC class I genes in HPV16 tumorigenic cells is partly due to HPV16E7 associated with the MHC class I promoter and repressed chromatin activation. In this study, we further demonstrated that HPV16E7 is physically associated with a putative RXR{beta} binding motif (GGTCA) of the proximal promoter of the MHC class I genes by using reporter transcriptional assays and chromatin immunoprecipitation assays. Our data also provide evidence that HPV16E7 inhibits TNF-{alpha}-induced up-regulation of MHC class I transcription by impaired nuclear translocation of NF-{kappa}B. More importantly, CaSki tumor cells treated with TSA and transfected with the constitutively active mutant form of IKK-{alpha} (which can activate NF-{kappa}B directly) showed a maximal level of up-regulation of MHC-I expression. Taken together, our results suggest that HPV16E7 may employ two independent mechanisms to ensure that either the constitutive or inducible transcription of MHC class I genes is down-regulated.

Authors:
; ;  [1];  [1]
  1. Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan (China)
Publication Date:
OSTI Identifier:
22199841
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 388; Journal Issue: 2; Other Information: Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; CHROMATIN; GENE REGULATION; GENES; INTERACTIONS; MUTANTS; PROMOTERS; TRANSCRIPTION; TRANSLOCATION; TUMOR CELLS

Citation Formats

Li, Hui, Zhan, TaiLan, Li, Chang, Liu, Mugen, Wang, Qing K., E-mail: qkwang@mail.hust.edu.cn, and Center for Cardiovascular Genetics, Cleveland Clinic, Cleveland, OH 44195. Repression of MHC class I transcription by HPV16E7 through interaction with a putative RXR{beta} motif and NF-{kappa}B cytoplasmic sequestration. United States: N. p., 2009. Web. doi:10.1016/J.BBRC.2009.08.019.
Li, Hui, Zhan, TaiLan, Li, Chang, Liu, Mugen, Wang, Qing K., E-mail: qkwang@mail.hust.edu.cn, & Center for Cardiovascular Genetics, Cleveland Clinic, Cleveland, OH 44195. Repression of MHC class I transcription by HPV16E7 through interaction with a putative RXR{beta} motif and NF-{kappa}B cytoplasmic sequestration. United States. https://doi.org/10.1016/J.BBRC.2009.08.019
Li, Hui, Zhan, TaiLan, Li, Chang, Liu, Mugen, Wang, Qing K., E-mail: qkwang@mail.hust.edu.cn, and Center for Cardiovascular Genetics, Cleveland Clinic, Cleveland, OH 44195. 2009. "Repression of MHC class I transcription by HPV16E7 through interaction with a putative RXR{beta} motif and NF-{kappa}B cytoplasmic sequestration". United States. https://doi.org/10.1016/J.BBRC.2009.08.019.
@article{osti_22199841,
title = {Repression of MHC class I transcription by HPV16E7 through interaction with a putative RXR{beta} motif and NF-{kappa}B cytoplasmic sequestration},
author = {Li, Hui and Zhan, TaiLan and Li, Chang and Liu, Mugen and Wang, Qing K., E-mail: qkwang@mail.hust.edu.cn and Center for Cardiovascular Genetics, Cleveland Clinic, Cleveland, OH 44195},
abstractNote = {Down-regulation of transcription of the MHC class I genes in HPV16 tumorigenic cells is partly due to HPV16E7 associated with the MHC class I promoter and repressed chromatin activation. In this study, we further demonstrated that HPV16E7 is physically associated with a putative RXR{beta} binding motif (GGTCA) of the proximal promoter of the MHC class I genes by using reporter transcriptional assays and chromatin immunoprecipitation assays. Our data also provide evidence that HPV16E7 inhibits TNF-{alpha}-induced up-regulation of MHC class I transcription by impaired nuclear translocation of NF-{kappa}B. More importantly, CaSki tumor cells treated with TSA and transfected with the constitutively active mutant form of IKK-{alpha} (which can activate NF-{kappa}B directly) showed a maximal level of up-regulation of MHC-I expression. Taken together, our results suggest that HPV16E7 may employ two independent mechanisms to ensure that either the constitutive or inducible transcription of MHC class I genes is down-regulated.},
doi = {10.1016/J.BBRC.2009.08.019},
url = {https://www.osti.gov/biblio/22199841}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 2,
volume = 388,
place = {United States},
year = {Fri Oct 16 00:00:00 EDT 2009},
month = {Fri Oct 16 00:00:00 EDT 2009}
}