ArticleOncology letters2019
VDAC1 is regulated by BRD4 and contributes to JQ1 resistance in breast cancer.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- BET inhibition unmasks a targetable glycolytic dependency through a HIF1α stabilization and driven transcriptional program in a defined subset of triple-negative breast Cancer.Cell death discovery · 2026Article
- A prognostic model for breast cancer based on mitochondria-associated endoplasmic reticulum membrane (MAM) signature genes.Discover oncology · 2026Article
- MBD3 increased expression by BRD4 and facilitated castration-resistant prostate cancer cell proliferation by inhibiting PTEN.Discover oncology · 2026Article
- LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications.Heliyon · 2025Article
- BET inhibitors (BETi) influence oxidative phosphorylation metabolism by affecting mitochondrial dynamics leading to alterations in apoptotic pathways in triple-negative breast cancer (TNBC) cells.Cell proliferation · 2024Article
- Construction of a prognostic score model for breast cancer based on multi-omics analysis of study on bone metastasis.Translational cancer research · 2024Article
- Role and regulation of FOXO3a: new insights into breast cancer therapy.Frontiers in pharmacology · 2024Review
- Effects of arginine on coenzyme-Q10 micelle uptake for mitochondria-targeted nanotherapy in phenylketonuria.Drug delivery and translational research · 2024Article
- The expression ofFrontiers in endocrinology · 2024Article
- Integrative analysis of the prognostic value and immune microenvironment of mitophagy-related signature for multiple myeloma.BMC cancer · 2023Article
- BETi enhance ATGL expression and its lipase activity to exert their antitumoral effects in triple-negative breast cancer (TNBC) cells.Journal of experimental & clinical cancer research : CR · 2023Article
- Lidocaine promotes apoptosis in breast cancer cells by affecting VDAC1 expression.BMC anesthesiology · 2022Article
- Overexpressed VDAC1 in breast cancer as a novel prognostic biomarker and correlates with immune infiltrates.World journal of surgical oncology · 2022Article
- Chloride Channels and Transporters: Roles beyond Classical Cellular Homeostatic pH or Ion Balance in Cancers.Cancers · 2022Review
- Functional Roles of Bromodomain Proteins in Cancer.Cancers · 2021Review
- VDAC Modulation of Cancer Metabolism: Advances and Therapeutic Challenges.Frontiers in physiology · 2021Review
- The emerging role of BET inhibitors in breast cancer.Breast (Edinburgh, Scotland) · 2020Review
- The epigenetic regulators and metabolic changes in ferroptosis-associated cancer progression.Molecular cancer · 2020Review
- Caveolin-2 is regulated by BRD4 and contributes to cell growth in pancreatic cancer.Cancer cell international · 2020Article
- Relevance of Membrane Contact Sites in Cancer Progression.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-dependent anion channels (VDACs) are situated in the outer membrane of the mitochondria and serve as gatekeepers that control metabolite and ion exchange between the cytosol and mitochondria. VDAC1 is one of the most studied members of the VDAC protein family and is overexpressed in multiple types of cancer. However, the specific biological function and regulatory mechanism of VDAC1 in breast cancer remains unclear. The present study investigated the biological role of VDAC1 in breast cancer cells using an MTS assay. The association of clinicopathological features with VDAC1 in breast cancer was analyzed by Gene Expression Profiling Interactive Analysis. The regulatory mechanism of VDAC1 was determined by cell transfection, western blot analysis, reverse transcription-quantitative (q)PCR analysis, chromatin immunoprecipitation (ChIP) and ChIP-qPCR analysis. The results of the present study demonstrated that VDAC1 promoted breast cancer proliferation and was associated with a poor prognosis in patients with breast cancer. Additionally, it was observed that the expression of VDAC1 could be decreased by the bromodomain inhibitor (JQ1), and bromodomain-containing protein 4 (BRD4) was indicated to be a regulator of VDAC1. Furthermore, results suggested that VDAC1 may be involved in the resistance of breast cancer to JQ1. Collectively, the present findings uncovered important aspects of the function of VDAC1 in the tumor progression of breast cancer, and may provide a basis for potential therapeutic strategies for the treatment of breast cancer.
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