ArticleCancer biology & therapy2018
Targeting BRD4 proteins suppresses the growth of NSCLC through downregulation of eIF4E expression.
Article in Cancer biology & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- AI-Driven Combination Therapy for Counteracting Dysregulated Genes in Lung Adenocarcinoma: Contribution-Aware Metaheuristic for Drug Repurposing.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Functional drug screening of tumor organoids on an active-matrix digital microfluidic chip for cancer precision medicine.Microsystems & nanoengineering · 2026Article
- Inhibition of BRD4 sensitizes NSCLC cells to osimertinib by suppressing APT1 and promoting MST1 palmitoylation.Cell death discovery · 2025Article
- A Combination of CPI-0610 and SAHA Induces Apoptosis through STAT3 and p38 Signalling Pathways in Diffuse Large B-cell Lymphoma Cells.Current medicinal chemistry · 2025Article
- LncRNA GAS5 regulated by FTO-mediated m6A demethylation promotes autophagic cell death in NSCLC by targeting UPF1/BRD4 axis.Molecular and cellular biochemistry · 2024Article
- Circular RNA in Non-small Cell Lung Carcinoma: Identification of Targets and New Treatment Modalities.Cancer genomics & proteomics · 2023Review
- Biological functions and research progress of eIF4E.Frontiers in oncology · 2023Review
- Comprehensive analysis of the prognosis and immune infiltrates for the BET protein family reveals the significance of BRD4 in glioblastoma multiforme.Frontiers in cell and developmental biology · 2023Article
- Susceptibility of Lung Carcinoma Cells to Nanostructured Lipid Carrier of ARV-825, a BRD4 Degrading Proteolysis Targeting Chimera.Pharmaceutical research · 2022Article
- Roles of Bromodomain Extra Terminal Proteins in Metabolic Signaling and Diseases.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Targeting sphingosine kinase 1/2 by a novel dual inhibitor SKI-349 suppresses non-small cell lung cancer cell growth.Cell death & disease · 2022Article
- PLEK2 promotes the proliferation and migration of non-small cell lung cancer cells in a BRD4-dependent manner.Molecular biology reports · 2022Article
- Epigenetic readers and lung cancer: the rs2427964C>T variant of the bromodomain and extraterminal domain gene BRD3 is associated with poorer survival outcome in NSCLC.Molecular oncology · 2022Article
- Circ_0000376 downregulation inhibits the progression of non-small cell lung cancer by mediating the miR-488-3p/BRD4 axis and the PI3K/PKB signaling pathway.Histology and histopathology · 2021Article
- BRD4 targeting nanotherapy prevents lipopolysaccharide induced acute respiratory distress syndrome.International journal of pharmaceutics · 2021Article
- Trichostatin A downregulates bromodomain and extra-terminal proteins to suppress osimertinib resistant non-small cell lung carcinoma.Cancer cell international · 2021Article
- MKL1-induced lncRNA SNHG18 drives the growth and metastasis of non-small cell lung cancer via the miR-211-5p/BRD4 axis.Cell death & disease · 2021Article
- Anticancer Effects of I-BET151, an Inhibitor of Bromodomain and Extra-Terminal Domain Proteins.Frontiers in oncology · 2021Review
- BRD4 inhibition promotes TRAIL-induced apoptosis by suppressing the transcriptional activity of NF-κB in NSCLC.International journal of medical sciences · 2021Article
- BRDT is a novel regulator of eIF4EBP1 in renal cell carcinoma.Oncology reports · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is the leading cause of cancer-related death worldwide. Bromodomain and extraterminal domain (BET) proteins act as epigenome readers for gene transcriptional regulation. Among BET family members, BRD4 was well studied, but for its mechanism in non-small cell lung carcinoma has not been elucidated. eIF4E regulates gene translation and has been proved to play an important role in the progression of lung cancer. In this study, we first confirmed that BET inhibitors JQ1 and I-BET151 suppressed the growth of NSCLCs, in parallel with downregulated eIF4E expression. Then we found that knockdown of BRD4 expression using siRNAs inhibited the growth of NSCLCs as well as decreased eIF4E protein levels. Moreover, overexpression of eIF4E partially abrogated the growth inhibitory effect of JQ1, while knockdown of eIF4E enhanced the inhibitory effect of JQ1. Furthermore, JQ1 treatment or knockdown of BRD4 expression decreased eIF4E mRNA levels and inhibited its promoter activity by luciferase reporter assay. JQ1 treatment significantly decreased the binding of eIF4E promoter with BRD4. Finally, JQ1 inhibited the growth of H460 tumors in parallel with downregulated eIF4E mRNA and protein levels in a xenograft mouse model. These findings suggest that inhibition of BET by JQ1, I-BET151, or BRD4 silencing suppresses the growth of non-small cell lung carcinoma through decreasing eIF4E transcription and subsequent mRNA and protein expression. Considering that BET regulates gene transcription epigenetically, our findings not only reveal a new mechanism of BET-regulated eIF4E in lung cancer, but also indicate a novel strategy by co-targeting eIF4E for enhancing BET-targeted cancer therapy.
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