ArticleThe Journal of experimental medicine2020
PRDM16 suppresses HIF-targeted gene expression in kidney cancer.
Article in The Journal of experimental medicine, 2020. 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.
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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, 46 citations in OpenAlex.
- PRDM16 as a Multifaceted Pharmacological Target in Kidney Diseases: From Epigenetic Mechanisms to Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Oxalate induces proliferation and mitochondrial metabolism in select clear cell renal cell carcinoma cell lines.BMC cancer · 2026Article
- Integrative analysis of nanopore direct RNA sequencing data reveals a global impact of pseudouridylation on mNPJ precision oncology · 2026Article
- PRDM16 Drives Thyroid Cancer Differentiation via a TRIM58-MVP Axis to Suppress MAPK and PI3K/AKT Signaling.International journal of biological sciences · 2026Article
- Article
- Overexpression of PRDM16 attenuates acute kidney injury progression: genetic and pharmacological approaches.MedComm · 2024Article
- Identification of a signature of histone modifiers in kidney renal clear cell carcinoma.Aging · 2024Article
- Article
- Extensive intratumor regional epigenetic heterogeneity in clear cell renal cell carcinoma targets kidney enhancers and is associated with poor outcome.Clinical epigenetics · 2023Article
- The Role of Histone Modification in DNA Replication-Coupled Nucleosome Assembly and Cancer.International journal of molecular sciences · 2023Review
- Article
- Identification of the enhancer RNAs related to tumorgenesis of pituitary neuroendocrine tumors.Frontiers in endocrinology · 2023Article
- Identifying Tumor-Associated Genes from Bilayer Networks of DNA Methylation Sites and RNAs.Life (Basel, Switzerland) · 2022Article
- Genes associated with diagnosis and prognosis of Burkitt lymphoma.IET systems biology · 2022Article
- LINC00589-dominated ceRNA networks regulate multiple chemoresistance and cancer stem cell-like properties in HER2NPJ breast cancer · 2022Article
- The evolving view of thermogenic fat and its implications in cancer and metabolic diseases.Signal transduction and targeted therapy · 2022Review
- PRDM16 Regulating Adipocyte Transformation and Thermogenesis: A Promising Therapeutic Target for Obesity and Diabetes.Frontiers in pharmacology · 2022Review
- MECOM/PRDM3 and PRDM16 Serve as Prognostic-Related Biomarkers and Are Correlated With Immune Cell Infiltration in Lung Adenocarcinoma.Frontiers in oncology · 2022Article
- Prognostic and Diagnostic Values of Semaphorin 5B and Its Correlation With Tumor-Infiltrating Immune Cells in Kidney Renal Clear-Cell Carcinoma.Frontiers in genetics · 2022Article
- Analysis of m6A RNA Methylation-Related Genes in Liver Hepatocellular Carcinoma and Their Correlation with Survival.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Analysis of transcriptomic data demonstrates extensive epigenetic gene silencing of the transcription factor PRDM16 in renal cancer. We show that restoration of PRDM16 in RCC cells suppresses in vivo tumor growth. RNaseq analysis reveals that PRDM16 imparts a predominantly repressive effect on the RCC transcriptome including suppression of the gene encoding semaphorin 5B (SEMA5B). SEMA5B is a HIF target gene highly expressed in RCC that promotes in vivo tumor growth. Functional studies demonstrate that PRDM16's repressive properties, mediated by physical interaction with the transcriptional corepressors C-terminal binding proteins (CtBP1/2), are required for suppression of both SEMA5B expression and in vivo tumor growth. Finally, we show that reconstitution of RCC cells with a PRDM16 mutant unable to bind CtBPs nullifies PRDM16's effects on both SEMA5B repression and tumor growth suppression. Collectively, our data uncover a novel epigenetic basis by which HIF target gene expression is amplified in kidney cancer and a new mechanism by which PRDM16 exerts its tumor suppressive effects.
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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.