Repression of MHC class I transcription by HPV16E7 through interaction with a putative RXR{beta} motif and NF-{kappa}B cytoplasmic sequestration
- 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)
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.
- OSTI ID:
- 22199841
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 388, 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); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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