ArticleEpigenetics2012
CD1d induction in solid tumor cells by histone deacetylase inhibitors through inhibition of HDAC1/2 and activation of Sp1.
Article in Epigenetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- Epigenetic repression of hepatocyte FoxO1 disrupts local immune homeostasis and promotes liver inflammation.Hepatology (Baltimore, Md.) · 2026Article
- Facts and Hopes of Chimeric Antigen Receptor-Redirected NK T Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Review
- STAT3 and SPI1, may lead to the immune system dysregulation and heterotopic ossification in ankylosing spondylitis.BMC immunology · 2022Article
- Adoptive Immunotherapy With Engineered iNKT Cells to Target Cancer Cells and the Suppressive Microenvironment.Frontiers in medicine · 2022Review
- Review
- Targeting Neoepitopes to Treat Solid Malignancies: Immunosurgery.Frontiers in immunology · 2021Review
- Acetylation in Tumor Immune Evasion Regulation.Frontiers in pharmacology · 2021Review
- HDAC4 is expressed on multiple T cell lineages but dispensable for their development and function.Oncotarget · 2017Article
- Harnessing the Power of Invariant Natural Killer T Cells in Cancer Immunotherapy.Frontiers in immunology · 2017Review
- Histone deacetylase inhibitors enhance CD1d-dependent NKT cell responses to lymphoma.Cancer immunology, immunotherapy : CII · 2016Article
- Inhibitors of histone deacetylase 1 reverse the immune evasion phenotype to enhance T-cell mediated lysis of prostate and breast carcinoma cells.Oncotarget · 2016Article
- All-trans-retinoic acid and CD38 ligation differentially regulate CD1d expression and α-galactosylceramide-induced immune responses.Immunobiology · 2015Article
- Role and regulation of CD1d in normal and pathological B cells.Journal of immunology (Baltimore, Md. : 1950) · 2014Review
- Epigenetic induction of CD1d expression primes lung cancer cells for killing by invariant natural killer T cells.OncoimmunologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD1d is a MHC class-like molecule that presents glycolipids to natural killer T (NKT) cells, then regulates innate and adaptive immunity. The regulation of CD1d gene expression in solid tumors is still largely unknown. Gene expression can be epigenetically regulated by DNA methylation and histone acetylation. We found that histone deacetylase inhibitors, trichostatin A (TSA) and suberoylanilide hydroxamic acid (SAHA), induced CD1d gene expression in human (A549 and NCI-H292) and mouse (TC-1 and B16/F0) cancer cells. Simultaneous knockdown of HDAC1 and 2 induced CD1d gene expression. Sp1 inhibitor mitramycin A (MTM) blocked TSA- and SAHA-induced CD1d mRNA expression and Sp1 luciferase activity. Co-transfection of GAL4-Sp1 and Fc-luciferase reporters demonstrated that TSA and SAHA induced Sp1 luciferase reporter activity by enhancing Sp1 transactivation activity. The binding of Sp1 to CD1d promoter and histone H3 acetylation on Sp1 sites were increased by TSA and SAHA. These results indicate that TSA and SAHA could up-regulate CD1d expression in tumor cells through inhibition of HDAC1/2 and activation of Sp1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.