ArticleInternational journal of molecular sciences2022
JIB-04, a Pan-Inhibitor of Histone Demethylases, Targets Histone-Lysine-Demethylase-Dependent AKT Pathway, Leading to Cell Cycle Arrest and Inhibition of Cancer Stem-Like Cell Properties in Hepatocellular Carcinoma Cells.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- The KDM-family inhibitor JIB-04 sensitizes AML cells to venetoclax by inducing a ferroptosis-like phenotype.Blood neoplasia · 2026Article
- Chromatin chronicles: Unlocking the therapeutic potential of histone modifiers in hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2026Review
- Transcriptomic Signature and PROTAC Strategy Revealed Histone Lysine Demethylase as a Target of Anticancer Activity of Deferiprone.ACS omega · 2026Article
- Repositioning Antihistamine for Cancer Therapy: Clemizole as a Template for the Design of Liver Tissue-Targeting Epigenetic-Modifying Agents.Journal of medicinal chemistry · 2026Article
- hsa_circ_0006168 drives microglial activation in TNC via miR-99b-5p/KDM6B axis to promote central sensitization in migraine.The journal of headache and pain · 2026Article
- Unveiling the hidden regulators: how post-translational modifications influence the progression and treatment of hepatocellular carcinoma.Frontiers in oncology · 2026Review
- Transcriptomic Signature and PROTAC Strategy Revealed Histone Lysine Demethylase as a Target of Anticancer Activity of Deferiprone.bioRxiv : the preprint server for biology · 2025Article
- JIB-04 improves PPARγ expression and enhances adipogenic differentiation efficiency in human umbilical cord mesenchymal stem cells.Biochemistry and biophysics reports · 2025Article
- Review
- HADHA-mediated regulation of JAK/STAT3 signaling in glioblastoma: a metabolic-epigenetic axis.Cell death discovery · 2025Article
- Epigenetic targeting of MECOM/KRAS axis by JIB-04 impairs tumorigenesis and cisplatin resistance in MECOM-amplified ovarian cancer.Cell death discovery · 2025Article
- Epigenetic Dysregulation in Cancer: Implications for Gene Expression and DNA Repair-Associated Pathways.International journal of molecular sciences · 2025Review
- Epigenetic editing and epi-drugs: a combination strategy to simultaneously target KDM4 as a novel anticancer approach.Clinical epigenetics · 2025Article
- Heterochromatin fidelity is a therapeutic vulnerability in lymphoma and other human cancers.bioRxiv : the preprint server for biology · 2025Article
- Reversing inflammatory diseases via trained immunity: mechanisms, challenges, and prospects.Frontiers in immunology · 2025Review
- Metabolic modulation of histone acetylation mediated by HMGCL activates the FOXM1/β-catenin pathway in glioblastoma.Neuro-oncology · 2024Article
- Methylation of the JMJD2B epigenetic regulator differentially affects its ability to coactivate the ETV1 and JUN transcription factors.International journal of biochemistry and molecular biology · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
JIB-04, a pan-histone lysine demethylase (KDM) inhibitor, targets drug-resistant cells, along with colorectal cancer stem cells (CSCs), which are crucial for cancer recurrence and metastasis. Despite the advances in CSC biology, the effect of JIB-04 on liver CSCs (LCSCs) and the malignancy of hepatocellular carcinoma (HCC) has not been elucidated yet. Here, we showed that JIB-04 targeted KDMs, leading to the growth inhibition and cell cycle arrest of HCC, and abolished the viability of LCSCs. JIB-04 significantly attenuated CSC tumorsphere formation, growth, relapse, migration, and invasion in vitro. Among KDMs, the deficiency of
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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.