ArticleInternational journal of oncology2018
Genome-wide transcriptional analysis of BRD4-regulated genes and pathways in human glioma U251 cells.
Article in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Targeting BRD4-A Promising Therapeutic Option for Glioblastoma?International journal of molecular sciences · 2026Review
- The chordoid gliomaScience signaling · 2025Article
- Unique vulnerability of RAC1-mutant melanoma to combined inhibition of CDK9 and immune checkpoints.Oncogene · 2024Article
- MZ1, a BRD4 inhibitor, exerted its anti-cancer effects by suppressing SDC1 in glioblastoma.BMC cancer · 2024Article
- Exploring new roles for RNA-binding proteins in epigenetic and gene regulation.Current opinion in genetics & development · 2024Review
- Bromodomain and Extraterminal Domain (BET) Protein Inhibition Hinders Glioblastoma Progression by Inducing Autophagy-Dependent Differentiation.International journal of molecular sciences · 2023Article
- Biomolecular condensates: Formation mechanisms, biological functions, and therapeutic targets.MedComm · 2023Review
- BRD4 promotes resection and homology-directed repair of DNA double-strand breaks.Nature communications · 2022Article
- SWAN pathway-network identification of common aneuploidy-based oncogenic drivers.Nucleic acids research · 2022Article
- Bromodomain-containing protein 4 activates cardiotrophin-like cytokine factor 1, an unfavorable prognostic biomarker, and promotes glioblastomaAnnals of translational medicine · 2022Article
- Inhibition of the bromodomain and extra-terminal family of epigenetic regulators as a promising therapeutic approach for gastric cancer.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- BRD4: An emerging prospective therapeutic target in glioma.Molecular therapy oncolytics · 2021Review
- Abnormal expression ofPeerJ · 2021Article
- Identification of Differentially Expressed Genes and Key Pathways in the Dorsal Root Ganglion After Chronic Compression.Frontiers in molecular neuroscience · 2020Article
- Article
- BRD4 and Cancer: going beyond transcriptional regulation.Molecular cancer · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bromodomain containing 4 (BRD4), a member of the bromodomain and extra-terminal family, has become a promising drug target for numerous types of cancer. BRD4 has been reported to be deregulated in gliomas; however, the precise molecular pathways regulated by BRD4 remained elusive. In the present study, BRD4 expression was silenced in the glioma cell line U251 and the results demonstrated that BRD4 knockdown attenuated cell proliferation and promoted cell apoptosis. A genome-wide analysis of BRD4-regulated transcripts in U251 cells was performed using microarray to reveal the possible molecular mechanism. A total of 3,529 differentially expressed genes were identified; 1,648 of these genes were upregulated and 1,881 were downregulated. The results of the gene ontology analysis revealed that these genes were mainly involved in membrane organization, mitotic cell cycle, cell division and DNA replication. Pathway analysis revealed that the pathways altered following BRD4 knockdown included multiple cellular processes, such as cell cycle and apoptosis. Candidate genes were identified through global signal transduction network analysis and were validated using reverse transcription-quantitative polymerase chain reaction and western blot analyses. The results demonstrated that BRD4 knockdown decreased the expression of KRAS proto-oncogene GTPase (KRAS). Downregulated KRAS expression in U251 cells restrained cell proliferation and promoted cell apoptosis, suggesting that the effect of BRD4 on glioma cells might occur through the Ras pathway. In conclusion, the present results confirmed the role of BRD4 in glioma and provided information for further exploration of the molecular mechanism of BRD4 in glioma development and progression.
Identifiers
What OpenQuestion holds
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.