ArticleAmerican journal of translational research2012
Genomic amplification and a role in drug-resistance for the KDM5A histone demethylase in breast cancer.
Article in American journal of translational research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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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Who cites it
84 citing papers in PubMed, 124 citations in OpenAlex.
- Investigation of DNA methylation levels before and after treatment in breast cancer patients receiving neoadjuvant chemotherapy.Breast cancer research and treatment · 2026Article
- Inhibition of KDM5A/B promotes antitumor innate immune responses in HHV-8/KSHV-positive B-cell lymphomas.Npj viruses · 2026Article
- KDM5D expression is lost in cisplatin‑resistant neuroblastoma cells.Oncology reports · 2026Article
- ERRα-KDM5C restrains STING enhancer activity to modulate type I interferon signaling in breast cancer progression.Cell death & disease · 2026Article
- Inhibition of KDM5A/B promotes antitumor innate immune responses in HHV-8/KSHV-positive B-cell lymphomas.bioRxiv : the preprint server for biology · 2026Article
- The KDM5A/HOXA5 axis regulates osteosarcoma progression via activating the Wnt/β-catenin pathway.European journal of medical research · 2025Article
- Decoding the Epigenome of Breast Cancer.International journal of molecular sciences · 2025Review
- KDM5A, a H3K4me3 demethylase, regulates skin wound healing by promoting M2 macrophage polarization via suppression of Socs1.Frontiers in physiology · 2025Article
- ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer.Cell reports · 2024Article
- The interaction between UBR7 and PRMT5 drives PDAC resistance to gemcitabine by regulating glycolysis and immune microenvironment.Cell death & disease · 2024Article
- KDM5 family as therapeutic targets in breast cancer: Pathogenesis and therapeutic opportunities and challenges.Molecular cancer · 2024Review
- RB1 loss induces quiescent state through downregulation of RAS signaling in mammary epithelial cells.Cancer science · 2024Article
- Identifying ligands for the PHD1 finger of KDM5A through high-throughput screening.RSC chemical biology · 2024Article
- Domain architecture and protein-protein interactions regulate KDM5A recruitment to the chromatin.Epigenetics · 2023Review
- MicroRNA-495: a therapeutic and diagnostic tumor marker.Journal of molecular histology · 2023Review
- BRWD3 promotes KDM5 degradation to maintain H3K4 methylation levels.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Dysregulated Signalling Pathways Driving Anticancer Drug Resistance.International journal of molecular sciences · 2023Review
- BRWD3 promotes KDM5 degradation to maintain H3K4 methylation levels.bioRxiv : the preprint server for biology · 2023Article
- KDM5 Lysine Demethylases in Pathogenesis, from Basic Science Discovery to the Clinic.Advances in experimental medicine and biology · 2023Article
- Epigenetically programmed resistance to chemo- and immuno-therapies.Advances in cancer research · 2023Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lysine-specific demethylase 5A (KDM5A), an enzyme that removes activating H3K4 di- and trimethylation marks, plays critical roles in controlling transcription and chromatin architecture, yet its biological functions largely remain uncharacterized, particularly in the context of human cancer. In the present study, we found that the KDM5A gene was significantly amplified and over-expressed in various human tumors, including breast cancer. Reducing the expression of KDM5A by shRNA knockdown inhibited proliferation of KDM5A-amplified breast cancer cells. More importantly, we demonstrated that KDM5A over-expression was associated with breast cancer drug resistance. Furthermore, knockdown of KDM5A gene expression altered H3K4 methylation and induced upregulation of CDK inhibitors as well as genes mediating apoptotic cell death. Taken together, our study strongly links KDM5A histone demethylase activity to breast cancer proliferation and drug resistance, and suggests KDM5A is a potential target for breast cancer therapy.
Indexed as
Identifiers
22937203PMC3426386W1481251422What OpenQuestion 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 OpenQuestion graph.