ArticleCell death discovery2024
KDM5B promotes SMAD4 loss-driven drug resistance through activating DLG1/YAP to induce lipid accumulation in pancreatic ductal adenocarcinoma.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- The tumor microenvironment in pancreatic cancer: from composition to therapeutic targeting.Biochemical Society transactions · 2026Review
- SMAD4 Palmitoylation Drives a Metabolic-Transcriptional Circuit to Promote Tumorigenesis and Confers Radiosensitivity in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Identification of Novel Small-Molecule Inhibitors Targeting KDM5B and Evaluation of Their Antitumour Effects.Cancer medicine · 2026Article
- The RNA methylation modification as an immunometabolic regulatory hub in pancreatic cancer: from mechanistic insights to clinical translation perspectives.Molecular cancer · 2026Review
- KDM5B-driven glucose metabolic reprogramming promotes enzalutamide resistance in prostate cancer via the lactate/hnRNPA1 lactylation/AR-V7 axis.Molecular cancer · 2026Article
- DNMT3A p.R882C driven proliferation and anti-apoptotic effects in pancreatic cancer cells.Scientific reports · 2026Article
- The interplay between extracellular matrix remodeling and cellular lipid metabolic reprogramming in cancer: a review.Molecular biology reports · 2025Review
- Review
- Acetylated KIAA1429 by TIP60 facilitates metastasis and immune evasion of hepatocellular carcinoma via N6-methyladenosine-KDM5B-mediated regulation of FoxO1.Cell death discovery · 2025Article
- Current advances and future directions in targeting histone demethylases for cancer therapy.Molecules and cells · 2025Review
- The Mechanism and Latest Progress of m6A Methylation in the Progression of Pancreatic Cancer.International journal of biological sciences · 2025Review
- Research progress on m6A and drug resistance in gastrointestinal tumors.Frontiers in pharmacology · 2025Review
- Article
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Authors and funding
9 authors.
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Abstract
Inactivated suppressor of mothers against decapentaplegic homolog (SMAD) 4 significantly affects cancer development in pancreatic ductal adenocarcinoma (PDAC). However, the contribution of smad4 loss to drug resistance in PDAC is largely undetermined. In the present study, we reported that the loss of SMAD4 endows PDAC cells the ability to drug resistance through upregulating histone lysine demethylase, Lysine-Specific Demethylase 5B (KDM5B, also known as JARID1B or PLU1). Upregulated KDM5B was found in PDAC, associated with poor prognosis and recurrence of PDAC patients. Upregulated KDM5B promotes PDAC tumor malignancy, i.e. cancer cells stemness and drug resistance in vitro and in vivo, while KDM5B knockout exerts opposite effects. Mechanistically, loss of Smad4-mediated upregulation of KDM5B promotes drug resistance through inhibiting the discs-large homolog 1 (DLG1), thereby facilitating nuclear translocation of YAP to induce de novo lipogenesis. Moreover, m
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