ArticleNature communications2024
BET inhibitors drive Natural Killer activation in non-small cell lung cancer via BRD4 and SMAD3.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- BET Inhibition Synergizes with RLR Signaling to Enhance Tumor Immunogenicity and T-cell Recognition.Cancer immunology research · 2026Article
- Therapeutic bacteria-trained NK cells confer long-term protection against cancer metastasis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Transcriptional networks weaving natural killer anti-tumor immune response.Molecular cancer · 2026Review
- Employing epigenetic protein degradation techniques to block CCL5-mediated photodynamic therapy via a programmed delivery platform.Signal transduction and targeted therapy · 2026Article
- Bromodomain and extra-terminal protein inhibitors modulate natural killer cell function and differentiation.Scientific reports · 2026Article
- BET Protein Degrader ZBC260 Induces Tumor Vascular Reprogramming Through Endothelial Cell Remodeling.Breast cancer (Dove Medical Press) · 2026Article
- Targeting bromodomain and extra-terminal proteins reprograms macrophages and inhibits breast cancer progression.Frontiers in immunology · 2026Article
- The role of NK cells in regulating tumorimmunity: current state, challenges and future strategies.Cancer cell international · 2025Review
- Epigenetic modifications in early stage lung cancer: pathogenesis, biomarkers, and early diagnosis.MedComm · 2025Review
- Bromodomain and extra-terminal proteins in solid tumors: regulators of immune microenvironment and emerging therapeutic targets.Frontiers in immunology · 2025Review
- Trained immunity in atherosclerosis: plasticity, metabolic-vascular axis, and AI-driven precision remodeling.Frontiers in immunology · 2025Review
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
Abstract
Non-small-cell lung carcinoma (NSCLC) is the most common lung cancer and one of the pioneer tumors in which immunotherapy has radically changed patients' outcomes. However, several issues are emerging and their implementation is required to optimize immunotherapy-based protocols. In this work, we investigate the ability of the Bromodomain and Extra-Terminal protein inhibitors (BETi) to stimulate a proficient anti-tumor immune response toward NSCLC. By using in vitro, ex-vivo, and in vivo models, we demonstrate that these epigenetic drugs specifically enhance Natural Killer (NK) cell cytotoxicity. BETi down-regulate a large set of NK inhibitory receptors, including several immune checkpoints (ICs), that are direct targets of the transcriptional cooperation between the BET protein BRD4 and the transcription factor SMAD3. Overall, BETi orchestrate an epigenetic reprogramming that leads to increased recognition of tumor cells and the killing ability of NK cells. Our results unveil the opportunity to exploit and repurpose these drugs in combination with immunotherapy.
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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.