ArticleInternational journal of cancer2012
CIITA is silenced by epigenetic mechanisms that prevent the recruitment of transactivating factors in rhabdomyosarcoma cells.
Article in International journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Epigenetic regulation of major histocompatibility complexes in gastrointestinal malignancies and the potential for clinical interception.Clinical epigenetics · 2024Pooled it
- Review
- Review
- CIITA/PRMT5 promote CD4BMC medicine · 2026Article
- Class II Major Histocompatibility Complex Transactivator (CIITA): A Master MHC-II Regulator Impacting Cancer and Beyond.Journal of immunotherapy and precision oncology · 2026Review
- CAR-T cell immunotherapy in rhabdomyosarcoma.Journal of translational medicine · 2026Review
- Article
- Targeting pattern recognition receptors for cancer therapy: Mechanisms and strategies.Acta pharmaceutica Sinica. B · 2025Review
- MHC Class II is Induced by IFNγ and Follows Three Distinct Patterns of Expression in Colorectal Cancer Organoids.Cancer research communications · 2023Article
- A review of the therapeutic potential of histone deacetylase inhibitors in rhabdomyosarcoma.Frontiers in oncology · 2023Review
- Pattern recognition receptors in health and diseases.Signal transduction and targeted therapy · 2021Review
- Autoantibody profiling of alveolar rhabdomyosarcoma patients unveils tumor-associated antigens with diagnostic and prognostic significance.Oncoimmunology · 2021Article
- Article
- Epigenetic priming restores the HLA class-I antigen processing machinery expression in Merkel cell carcinoma.Scientific reports · 2017Article
- Epigenetic modification and preliminary investigation of the mechanism of the immune evasion of HL-60 cells.Molecular medicine reports · 2015Article
- HDAC2 deregulation in tumorigenesis is causally connected to repression of immune modulation and defense escape.Oncotarget · 2015Article
- Overexpression of the skNAC gene in human rhabdomyosarcoma cells enhances their differentiation potential and inhibits tumor cell growth and spreading.Clinical & experimental metastasis · 2014Article
- Activation of ERα signaling differentially modulates IFN-γ induced HLA-class II expression in breast cancer cells.PloS one · 2014Article
- Exploiting tumor epigenetics to improve oncolytic virotherapy.Frontiers in genetics · 2013Review
- PML promotes MHC class II gene expression by stabilizing the class II transactivator.The Journal of cell biology · 2012Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Rhabdomyosarcomas (RMS) are highly malignant pediatric sarcomas. We have discovered that the gene encoding the major histocompatibilty complex class II transactivator, CIITA, is silenced in cells representing both major subtypes of RMS. Silencing of CIITA prevents the IFN-γ inducible expression of MHC class II genes in these cells. Overexpression of CIITA in these cells can restore MHC expression. We have found that IFN-γ signaling is intact in these cells, but pSTAT1 and IRF1 do not bind to the CIITA PIV promoter. The CIITA promoter is not hypermethylated in RD (ERMS) cells but does show a modestly enhanced methylation status in SJRH30 (ARMS) cells. We have found that histone acetylation, which normally increases on the CIITA PIV promoter following IFN-γ treatment, is blocked in both types of RMS cells. In RD cells, treatment with a histone deacetylase inhibitor (TSA) reverses the silencing of CIITA. In SJRH30 cells, treatment with DNA methyltransferase inhibitors and TSA cooperatively restores CIITA expression. Surprisingly, we have also shown that the expression of two components of the immunoproteasome, which are embedded in the class II locus, is stimulated by IFN-γ in certain RMS cells in the absence of stimulation by CIITA. CIITA overexpression can also activate the expression of these genes, indicating that the immunoproteasome genes LMP2 and LMP7 can be activated by both CIITA dependent and CIITA independent pathways.
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