ArticleOncotarget2013
KDM1 is a novel therapeutic target for the treatment of gliomas.
Article in Oncotarget, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 60 citations in OpenAlex.
- Enhancer of Zeste Homolog 2 (EZH2): From Glioblastoma Biology to Potential Epigenetic Therapy.International journal of molecular sciences · 2026Review
- Modulatory Effect of Curcumin on Expression of Methyltransferase/Demethylase in Colon Cancer Cells: Impact on wt p53, mutp53 and c-Myc.Molecules (Basel, Switzerland) · 2025Article
- KDM1A/LSD1 inhibition enhances chemotherapy response in ovarian cancer.Molecular carcinogenesis · 2024Article
- Pharmacological inhibition of the LIF/LIFR autocrine loop reveals vulnerability of ovarian cancer cells to ferroptosis.NPJ precision oncology · 2024Article
- Novel LIPA-Targeted Therapy for Treating Ovarian Cancer.Cancers · 2024Article
- Preclinical Development of Brain Permeable ERβ Agonist for the Treatment of Glioblastoma.Molecular cancer therapeutics · 2023Article
- Lysine-specific histone demethylase 1A (KDM1A/LSD1) inhibition attenuates DNA double-strand break repair and augments the efficacy of temozolomide in glioblastoma.Neuro-oncology · 2023Article
- Targeting the LSD1/KDM1 Family of Lysine Demethylases in Cancer and Other Human Diseases.Advances in experimental medicine and biology · 2023Review
- The function of histone methylation and acetylation regulators in GBM pathophysiology.Frontiers in oncology · 2023Review
- A First-in-Class Inhibitor of ER Coregulator PELP1 Targets ER+ Breast Cancer.Cancer research · 2022Article
- KDM1A inhibition augments the efficacy of rapamycin for the treatment of endometrial cancer.Cancer letters · 2022Article
- The Impact of Epigenetic Modifications on Adaptive Resistance Evolution in Glioblastoma.International journal of molecular sciences · 2021Review
- KDM1A inhibition is effective in reducing stemness and treating triple negative breast cancer.Breast cancer research and treatment · 2021Article
- PELP1 signaling contributes to medulloblastoma progression by regulating the NF-κB pathway.Molecular carcinogenesis · 2020Article
- Epigenetic regulation of cancer stem cell and tumorigenesis.Advances in cancer research · 2020Review
- Targeting of Histone Demethylases KDM5A and KDM6B Inhibits the Proliferation of Temozolomide-Resistant Glioblastoma Cells.Cancers · 2019Article
- Novel dual-action prodrug triggers apoptosis in glioblastoma cells by releasing a glutathione quencher and lysine-specific histone demethylase 1A inhibitor.Journal of neurochemistry · 2019Article
- Pharmacological Inhibition of LSD1 for Cancer Treatment.Molecules (Basel, Switzerland) · 2018Review
- Differential Effects of Estrogen Receptor β Isoforms on Glioblastoma Progression.Cancer research · 2018Article
- Epigenetic Targeting of Glioblastoma.Frontiers in oncology · 2018Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Glioma development is a multistep process, involving alterations in genetic and epigenetic mechanisms. Understanding the mechanisms and enzymes that promote epigenetic changes in gliomas are urgently needed to identify novel therapeutic targets. We examined the role of histone demethylase KDM1 in glioma progression. KDM1 was overexpressed in gliomas and its expression positively correlated with histological malignancy. Knockdown of KDM1 expression or its pharmacological inhibition using pargyline or NCL-1 significantly reduced the proliferation of glioma cells. Inhibition of KDM1 promoted up regulation of the p53 target genes p21 and PUMA. Patient-derived primary GBM cells expressed high levels of KDM1 and pharmacological inhibition of KDM1 decreased their proliferation. Further, KDM1 inhibition reduced the expression of stemness markers CD133 and nestin in GBM cells. Mouse xenograft assays revealed that inhibition of KDM1 significantly reduced glioma xenograft tumor growth. Inhibition of KDM1 increased levels of H3K4-me2 and H3K9-Ac histone modifications, reduced H3K9-me2 modification and promoted expression of p53 target genes (p21 and PUMA), leading to apoptosis of glioma xenograft tumors. Our results suggest that KDM1 is overexpressed in gliomas and could be a potential therapeutic target for the treatment of gliomas.
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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.