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:
-
- 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}
}