ArticleOncogene2004
Epigenetic inactivation of class II transactivator (CIITA) is associated with the absence of interferon-gamma-induced HLA-DR expression in colorectal and gastric cancer cells.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Epigenetic regulation of major histocompatibility complexes in gastrointestinal malignancies and the potential for clinical interception.Clinical epigenetics · 2024Pooled it
- Review
- Class II Major Histocompatibility Complex Transactivator (CIITA): A Master MHC-II Regulator Impacting Cancer and Beyond.Journal of immunotherapy and precision oncology · 2026Review
- CIITA was involved in regulating ACSL4-dependent ferroptosis in gastric cancer cells.Molecular and cellular biochemistry · 2026Article
- Iron Dyshomeostasis and Divergent Antigen Presentation Remodeling in Bronchiectasis: A Dual-Dataset Transcriptomic Analysis.Journal of inflammation research · 2026Article
- Biological mechanism and immune response of MHC-II expression in tumor cells.Cancer biology & medicine · 2025Review
- MHC Class II is Induced by IFNγ and Follows Three Distinct Patterns of Expression in Colorectal Cancer Organoids.Cancer research communications · 2023Article
- Interferons and Resistance Mechanisms in Tumors and Pathogen-Driven Diseases-Focus on the Major Histocompatibility Complex (MHC) Antigen Processing Pathway.International journal of molecular sciences · 2023Review
- Identification of immune activation-related gene signature for predicting prognosis and immunotherapy efficacy in lung adenocarcinoma.Frontiers in immunology · 2023Article
- Dysregulation in IFN-γ signaling and response: the barricade to tumor immunotherapy.Frontiers in immunology · 2023Review
- Article
- BCG-Induced Tumor Immunity Requires Tumor-Intrinsic CIITA Independent of MHC-II.Cancer immunology research · 2022Article
- Regulation of the antigen presentation machinery in cancer and its implication for immune surveillance.Biochemical Society transactions · 2022Review
- Luteolin Causes 5'CpG Demethylation of the Promoters of TSGs and Modulates the Aberrant Histone Modifications, Restoring the Expression of TSGs in Human Cancer Cells.International journal of molecular sciences · 2022Article
- Molecular Biomarker of Drug Resistance Developed From Patient-Derived Organoids Predicts Survival of Colorectal Cancer Patients.Frontiers in oncology · 2022Article
- Distinct Molecular Mechanisms of Altered HLA Class II Expression in Malignant Melanoma.Cancers · 2021Article
- Challenges of Neoantigen Targeting in Lynch Syndrome and Constitutional Mismatch Repair Deficiency Syndrome.Cancers · 2021Review
- Why do intestinal epithelial cells express MHC class II?Immunology · 2021Review
- Interferons in cancer immunoediting: sculpting metastasis and immunotherapy response.The Journal of clinical investigation · 2021Review
- Prognostic Immune-Related Analysis Based on Differentially Expressed Genes in Left- and Right-Sided Colon Adenocarcinoma.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tightly regulated at the level of transcription, expression of MHC class II molecules varies significantly among gastrointestinal cancers. High levels of MHC class II expression are often associated with a better prognosis, which is indicative of the involvement of CD4+ lymphocytes in tumor suppression, but the molecular mechanism by which MHC class II expression is regulated remains unclear. In the present study, we investigated the expression of one inducible MHC class II molecule, HLA-DR, and its coactivators in a panel of colorectal and gastric cancer cell lines. Interferon-gamma induced expression of HLA-DR in 14 of 20 cell lines tested; the remaining six cell lines did not express HLA-DR. Analysis of the expression of transcription factors and coactivators associated with HLA-DR revealed that the loss of CIITA expression was closely associated with the absence of HLA-DR induction. Moreover, DNA methylation of the 5' CpG island of CIITA-PIV was detected in all cancer cells that lacked CIITA. The methylation and resultant silencing of CIITA-PIV depended on the activities of two DNA methyltransferases, DNMT1 and DNMT3B, and their genetic inactivation restored CIITA-PIV expression. It thus appears that CIITA methylation is a key mechanism that enables some gastrointestinal cancer cells to escape immune surveillance.
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Registered trials
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