ArticleLeukemia2024
CREB1 promotes expression of immune checkpoint HLA-E leading to immune escape in multiple myeloma.
Article in Leukemia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- HLA-E-Directed Accumulation of KIRInternational journal of molecular sciences · 2026Article
- The bacteroidal metabolite O-LysoPE facilitates hepatocyte-mediated immunosuppression in autoimmune hepatitis.Nature communications · 2026Article
- A fully human pan VL9 HLA-E TCRm antibody enables functional dissection of HLA-E biology and checkpoint signaling.iScience · 2026Article
- HLA-E as an Emerging Checkpoint and Biomarker in Personalized Cancer Immunotherapy.Current medical science · 2026Review
- Review
- Combinatorial treatment with donafenib and quercetin suppresses lipid metabolism in HepG2 cells by targeting the CREB1/DRP1/SREBP1 axis.Translational cancer research · 2026Article
- Article
- Regulation of stress tolerance by CREB1 sustains multiple myeloma cell survival.Cell death & disease · 2026Article
- Artificial neural network-based immune biomarker signature predicts pathological complete response to neoadjuvant chemotherapy in HER2-negative breast cancer.Frontiers in oncology · 2026Article
- Bioinformatics identification and experimental validation of hub genes associated with narcolepsy type 1.Journal of clinical and translational science · 2026Article
- A PSAT1 buff of YBX1 transcriptionally sustains HLA-E-mediated evasion of NK immunity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Comprehensive Bioinformatic Analysis Reveals Survival-Associated Hub Genes and MicroRNAs in Multiple Myeloma Patients.Iranian journal of biotechnology · 2025Article
- HLA-F regulates the proliferation of trophoblast via PKM2-dependent glycolysis in the pathogenesis of preeclampsia.Molecular medicine (Cambridge, Mass.) · 2025Article
- Article
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Authors and funding
8 authors.
Funding
Abstract
Multiple myeloma (MM) cells effectively escape anti-tumoral immunity to survive in the tumor microenvironment (TME). Herein, we identify non-classical major histocompatibility complex (MHC) class I molecule HLA-E as a major contributing factor in immune escape. Clinically, HLA-E expression correlates with aggressive disease features such as t(4;14) and CD56 expression and is induced by IFN-gamma (IFN-γ) in the TME. We discovered that HLA-E is regulated by cAMP responsive element binding protein 1 (CREB1) transcription factor by direct promoter binding; genomic and pharmacological inhibition of CREB1 reduced HLA-E levels even in the presence of IFN-γ or IFN-γ activating agents, such as immunomodulatory drugs and panobinostat. HLA-E binds to natural killer group 2A (NKG2A), delivering an inhibitor signal to natural killer (NK) cells. Treatment with a CREB1 inhibitor was able to restore NK cell-mediated cytotoxicity against MM cell lines and patient samples. In conclusion, our results strongly demonstrate that CREB1 inhibition promotes anti-tumoral immunity in MM by limiting HLA-E expression and enhancing the activity of NK cells.
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Registered trials
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