ArticleOncogene2016
Somatic human ZBTB7A zinc finger mutations promote cancer progression.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Epigenetic control of metabolic identity across cell types.BMC genomics · 2025Article
- Transmembrane emp24 domain-containing protein 3 promotes the malignant progression of glioma by regulating the ZBTB7A signaling axis.Molecular biomedicine · 2025Article
- Exploring the role of glycolysis in the pathogenesis of erectile dysfunction in diabetes.Translational andrology and urology · 2025Article
- Protein structural context of cancer mutations reveals molecular mechanisms and candidate driver genes.Cell reports · 2024Article
- ZBTB7A regulates LncRNA HOTAIR-mediated ELAVL1/SOX17 axis to inhibit malignancy and angiogenesis in endometrial carcinoma.Journal of cancer research and clinical oncology · 2024Article
- U3 snoRNA-mediated degradation of ZBTB7A regulates aerobic glycolysis in isocitrate dehydrogenase 1 wild-type glioblastoma cells.CNS neuroscience & therapeutics · 2023Article
- Insights into the pleiotropic roles of ZNF703 in cancer.Heliyon · 2023Review
- Multiomic analysis of cohesin reveals that ZBTB transcription factors contribute to chromatin interactions.Nucleic acids research · 2023Article
- The Roles of Zinc Finger Proteins in Colorectal Cancer.International journal of molecular sciences · 2023Review
- The zinc figure protein ZNF575 impairs colorectal cancer growth via promoting p53 transcription.Oncology research · 2023Article
- AML1/ETO and its function as a regulator of gene transcription via epigenetic mechanisms.Oncogene · 2021Review
- An order independent algorithm for inferring gene regulatory network using quantile value for conditional independence tests.Scientific reports · 2021Article
- The Prognostic Value of the DNA Repair Gene Signature in Head and Neck Squamous Cell Carcinoma.Frontiers in oncology · 2021Article
- ZBTB7A, a potential biomarker for prognosis and immune infiltrates, inhibits progression of endometrial cancer based on bioinformatics analysis and experiments.Cancer cell international · 2020Article
- The Emerging Role of MicroRNAs in Regulating the Drug Response of Cholangiocarcinoma.Biomolecules · 2020Review
- De novo ZBTB7A variant in a patient with macrocephaly, intellectual disability, and sleep apnea: implications for the phenotypic development in 19p13.3 microdeletions.Journal of human genetics · 2020Article
- Seven-Gene Signature Based on Glycolysis Is Closely Related to the Prognosis and Tumor Immune Infiltration of Patients With Gastric Cancer.Frontiers in oncology · 2020Article
- The multi-faceted functioning portrait of LRF/ZBTB7A.Human genomics · 2019Review
- Recurrent mutations at estrogen receptor binding sites alter chromatin topology and distal gene expression in breast cancer.Genome biology · 2018Article
- ZBTB7A governs estrogen receptor alpha expression in breast cancer.Journal of molecular cell biology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
We recently reported that ZBTB7A is a bona fide transcription repressor of key glycolytic genes and its downregulation in human cancer contributes to tumor metabolism. As reduced expression of ZBTB7A is found only in a subset of human cancers, we explored alternative mechanisms of its inactivation by mining human cancer genome databases. We discovered recurrent somatic mutations of ZBTB7A in multiple types of human cancers with a marked enrichment of mutations within the zinc finger domain. Functional characterization of the mutants demonstrated that mutations within the zinc finger region of ZBTB7A invariably resulted in loss of function. As a consequence, the glycolytic genes were markedly upregulated in cancer cells harboring ZBTB7A zinc finger mutation, leading to increased glycolysis and proliferation. Our study uncovers the loss-of-function mutation in ZBTB7A as a novel mechanism causing elevated glycolysis in human cancer, which carries important therapeutic implication.
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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.