ArticleJournal of experimental & clinical cancer research : CR2018
BRD7 expression and c-Myc activation forms a double-negative feedback loop that controls the cell proliferation and tumor growth of nasopharyngeal carcinoma by targeting oncogenic miR-141.
Article in Journal of experimental & clinical cancer research : CR, 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, 38 citations in OpenAlex.
- Targeted demethylation of the BRD7 promoter based on CRISPR/dCas9 system inhibits the malignant progression of nasopharyngeal carcinoma.Clinical and translational medicine · 2026Article
- The LFR-SWI/SNF complex: A chromatin wrench safeguarding cellular quiescence in theProceedings of the National Academy of Sciences of the United States of America · 2025Article
- VPS37A Activates the Autophagy-Lysosomal Pathway for TNFR1 Degradation and Induces NF-Oncology research · 2025Article
- BRD7 Inhibited Immune Escape in Nasopharyngeal Carcinoma via Inhibiting PD-L1 Expression.International journal of biological sciences · 2025Article
- BRD7 enhances the radiosensitivity of nasopharyngeal carcinoma cells by negatively regulating USP5/METTL3 axis-mediated homologous recombination repair.International journal of biological sciences · 2024Article
- Activation of MEK-ERK-c-MYC signaling pathway promotes splenic M2-like macrophage polarization to inhibit PHcH-liver cirrhosis.Frontiers in immunology · 2024Article
- Rational Design and Development of Selective BRD7 Bromodomain Inhibitors and Their Activity in Prostate Cancer.Journal of medicinal chemistry · 2023Article
- BRD7 inhibits enhancer activity and expression of BIRC2 to suppress tumor growth and metastasis in nasopharyngeal carcinoma.Cell death & disease · 2023Article
- Bromodomain (BrD) Family Members as Regulators of Cancer Stemness-A Comprehensive Review.International journal of molecular sciences · 2023Review
- Yin Yang 1 suppresses tumor invasion and metastasis in nasopharyngeal carcinoma by negatively regulating eIF4E transcriptional activity and expression.American journal of cancer research · 2023Article
- Leveraging a gene signature associated with disulfidptosis identified by machine learning to forecast clinical outcomes, immunological heterogeneities, and potential therapeutic targets within lower-grade glioma.Frontiers in immunology · 2023Article
- Splicing factor derived circular RNA circCAMSAP1 accelerates nasopharyngeal carcinoma tumorigenesis via a SERPINH1/c-Myc positive feedback loop.Molecular cancer · 2022Article
- MYC-activated RNA N6-methyladenosine reader IGF2BP3 promotes cell proliferation and metastasis in nasopharyngeal carcinoma.Cell death discovery · 2022Article
- BRD7 Stabilizes P53 via Dephosphorylation of MDM2 to Inhibit Tumor Growth in Breast Cancer Harboring Wild-type P53.Journal of Cancer · 2022Article
- Review
- Long non-coding RNA MIR200CHG promotes breast cancer proliferation, invasion, and drug resistance by interacting with and stabilizing YB-1.NPJ breast cancer · 2021Article
- BRD7 inhibits tumor progression by positively regulating the p53 pathway in hepatocellular carcinoma.Journal of Cancer · 2021Article
- BRD7 Promotes Cell Proliferation and Tumor Growth Through Stabilization of c-Myc in Colorectal Cancer.Frontiers in cell and developmental biology · 2021Article
- BRD7 suppresses invasion and metastasis in breast cancer by negatively regulating YB1-induced epithelial-mesenchymal transition.Journal of experimental & clinical cancer research : CR · 2020Article
- CDK12 promotes papillary thyroid cancer progression through regulating the c-myc/β-catenin pathway.Journal of Cancer · 2020Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundmiR-141 is up-regulated and plays crucial roles in nasopharyngeal carcinoma (NPC). However, the molecular mechanism underlying the dysregulation of miR-141 is still obscure.
methodsThus, the ChIP-PCR was performed to identify the c-Myc-binding sites in miR-141 and BRD7. qRT-PCR, western blot and immunohistochemistry assays were used to detect the expression of miR-141 and its up/down stream molecules. The rescue experiments on the c-Myc/miR-141 axis were performed in vitro and in vivo.
resultsOur results showed that the levels of mature miR-141, pre-miR-141 and pri-miR-141 were downregulated in c-Myc knockdown NPC cells. Meanwhile, c-Myc transactivates the expression of miR-141 by binding its promoter region. Moreover, BRD7 was identified as a co-factor of c-Myc to negatively regulate the activation of c-Myc/miR-141 axis, as well as a direct target of c-Myc. Moreover, restoration of miR-141 in c-Myc knockdown NPC cells notably rescued the effect of c-Myc on cell proliferation and tumor growth, as well as the blocking of PTEN/AKT pathway. Additionally, the expression of c-Myc was positively correlated with that of miR-141 and the clinical stages of NPC patients and negatively associated with the expression of BRD7. Our findings demonstrated that BRD7 expression and c-Myc activation forms a negative feedback loop to control the cell proliferation and tumor growth by targeting miR-141.
conclusionsThese observations provide new mechanistic insights into the dysregulation of miR-141 expression and a promising therapeutic option for NPC.
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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.