ArticleCell death discovery2021
Histone demethylase KDM5A promotes tumorigenesis of osteosarcoma tumor.
Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- The Identification by Shotgun Proteomics with High-Resolution Tandem Mass-Spectrometry of Histone Isoforms' Hypermethylation Phenotype as a Hallmark Characteristic of Human-IDH-Mutant High-Grade Gliomas: Epigenetic Applications for Genotoxicity-Based Biomarkers and Cancer Therapy Targets.Journal of proteome research · 2025Article
- The KDM5A/HOXA5 axis regulates osteosarcoma progression via activating the Wnt/β-catenin pathway.European journal of medical research · 2025Article
- Drug tolerant persister cell plasticity in cancer: A revolutionary strategy for more effective anticancer therapies.Signal transduction and targeted therapy · 2024Review
- KDM5A/B contribute to HIV-1 latent infection and survival of HIV-1 infected cells.Antiviral research · 2024Article
- The emerging roles of histone demethylases in cancers.Cancer metastasis reviews · 2024Review
- Multiple Comprehensive Analyses Identify Lysine Demethylase KDM as a Potential Therapeutic Target for Pancreatic Cancer.International journal of medical sciences · 2024Article
- Review
- ITGB3 promotes cisplatin resistance in osteosarcoma tumors.Cancer medicine · 2023Article
- The role of ARL4C in predicting prognosis and immunotherapy drug susceptibility in pan-cancer analysis.Frontiers in pharmacology · 2023Article
- Entanglement of Methylation Changes and cGAS-STING Signaling in Non-Small-Cell Lung Cancer.Combinatorial chemistry & high throughput screening · 2023Article
- KDM5 Lysine Demethylases in Pathogenesis, from Basic Science Discovery to the Clinic.Advances in experimental medicine and biology · 2023Article
- Joining the PARty: PARP Regulation of KDM5A during DNA Repair (and Transcription?).BioEssays : news and reviews in molecular, cellular and developmental biology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Osteosarcoma is a primary bone malignancy with a high rate of recurrence and poorer prognosis. Therefore, it is of vital importance to explore novel prognostic molecular biomarkers and targets for more effective therapeutic approaches. Previous studies showed that histone demethylase KDM5A can increase the proliferation and metastasis of several cancers. However, the function of KDM5A in the carcinogenesis of osteosarcoma is not clear. In the current study, KDM5A was highly expressed in osteosarcoma than adjacent normal tissue. Knockdown of KDM5A suppressed osteosarcoma cell proliferation and induced apoptosis. Moreover, knockdown of KDM5A could increase the expression level of P27 (cell-cycle inhibitor) and decrease the expression of Cyclin D1. Furthermore, after knockout of KDM5A in osteosarcoma cells by CRISPR/Cas9 system, the tumor size and growth speed were inhibited in tumor-bearing nude mice. RNA-Seq of KDM5A-KO cells indicated that interferon, epithelial-mesenchymal transition (EMT), IL6/JAK/STAT3, and TNF-α/NF-κB pathway were likely involved in the regulation of osteosarcoma cell viability. Taken together, our research established a role of KDM5A in osteosarcoma tumorigenesis and progression.
Identifiers
What Socratic 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 Socratic graph.