ArticleThe Journal of clinical investigation2015
Histone demethylase JARID1C inactivation triggers genomic instability in sporadic renal cancer.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 47 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
47 citing papers in PubMed, 81 citations in OpenAlex.
- SNORA23-KDM5C epigenetic axis mediates dual DNA repair pathways to drive radioresistance in esophageal squamous cell carcinoma.Cell death and differentiation · 2026Article
- CT-Based Radiomics for Prediction of Molecular Markers in Clear Cell Renal Cell Carcinoma: A Comprehensive Review.Medicina (Kaunas, Lithuania) · 2026Review
- UTY (KDM6C) in Cancer: Epigenetic Regulation, Tumour Suppressor Functions, and Clinical Implications.Epigenomes · 2026Review
- Genetic Aberrations in Normal Tissues Adjacent to Biliary Tract Cancers.Biomedicines · 2025Article
- Review
- KDM5C and KDM5D mutations have different consequences in clear cell renal cell carcinoma cells.Communications biology · 2025Article
- Relationship Between Loss of Y Chromosome and Urologic Cancers: New Future Perspectives.Cancers · 2024Review
- Versatile JMJD proteins: juggling histones and much more.Trends in biochemical sciences · 2024Review
- Comparing the roles of sex chromosome-encoded protein homologs in gene regulation.Genes & development · 2024Review
- Recognition of Histone H3 Methylation States by the PHD1 Domain of Histone Demethylase KDM5A.ACS chemical biology · 2023Article
- RepID represses megakaryocytic differentiation by recruiting CRL4A-JARID1A at DAB2 promoter.Cell communication and signaling : CCS · 2023Article
- RepID represses megakaryocytic differentiation by recruiting CRL4A-JARID1A at DAB2 promoter.Research square · 2023Article
- KDM5 Lysine Demethylases in Pathogenesis, from Basic Science Discovery to the Clinic.Advances in experimental medicine and biology · 2023Article
- Article
- Review
- Review
- Biological Sex As a Critical Variable in CD4Antioxidants & redox signaling · 2022Review
- Chromatin Velocity reveals epigenetic dynamics by single-cell profiling of heterochromatin and euchromatin.Nature biotechnology · 2022Article
- KDM5A and KDM5B histone-demethylases contribute to HU-induced replication stress response and tolerance.Biology open · 2021Article
- The Dual Function of KDM5C in Both Gene Transcriptional Activation and Repression Promotes Breast Cancer Cell Growth and Tumorigenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
Corrections and comments
- Correction · 2016-11-01Error in Data ·
- Erratum issued
Authors and funding
17 authors at 4 institutions in 4 countries.
Funding
Abstract
Mutations in genes encoding chromatin-remodeling proteins are often identified in a variety of cancers. For example, the histone demethylase JARID1C is frequently inactivated in patients with clear cell renal cell carcinoma (ccRCC); however, it is largely unknown how JARID1C dysfunction promotes cancer. Here, we determined that JARID1C binds broadly to chromatin domains characterized by the trimethylation of lysine 9 (H3K9me3), which is a histone mark enriched in heterochromatin. Moreover, we found that JARID1C localizes on heterochromatin, is required for heterochromatin replication, and forms a complex with established players of heterochromatin assembly, including SUV39H1 and HP1α, as well as with proteins not previously associated with heterochromatin assembly, such as the cullin 4 (CUL4) complex adaptor protein DDB1. Transcription on heterochromatin is tightly suppressed to safeguard the genome, and in ccRCC cells, JARID1C inactivation led to the unrestrained expression of heterochromatic noncoding RNAs (ncRNAs) that in turn triggered genomic instability. Moreover, ccRCC patients harboring JARID1C mutations exhibited aberrant ncRNA expression and increased genomic rearrangements compared with ccRCC patients with tumors endowed with other genetic lesions. Together, these data suggest that inactivation of JARID1C in renal cancer leads to heterochromatin disruption, genomic rearrangement, and aggressive ccRCCs. Moreover, our results shed light on a mechanism that underlies genomic instability in sporadic cancers.
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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.