ArticleThe Journal of biological chemistry2013
Triptolide-induced cell death in pancreatic cancer is mediated by O-GlcNAc modification of transcription factor Sp1.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 59 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
59 citing papers in PubMed, 111 citations in OpenAlex.
- Tripterine Liposome Exerts Antitumor and Immunomodulatory Effects in Pancreatic Ductal Adenocarcinoma.MedComm · 2026Article
- The Link Between Endoplasmic Reticulum Stress and Lysosomal Dysfunction Under Oxidative Stress in Cancer Cells.Biomolecules · 2025Review
- Phosphofructokinase-1 in Cancer: A Promising Target for Diagnosis and Therapy.Recent patents on anti-cancer drug discovery · 2025Review
- Muscle Proteome Analysis of Facioscapulohumeral Dystrophy Patients Reveals a Metabolic Rewiring Promoting Oxidative/Reductive Stress Contributing to the Loss of Muscle Function.Antioxidants (Basel, Switzerland) · 2024Article
- A comprehensive review on phytochemicals in the treatment and prevention of pancreatic cancer: Focusing on their mechanism of action.Health science reports · 2024Article
- Antitumor mechanisms and future clinical applications of the natural product triptolide.Cancer cell international · 2024Review
- Review
- Specificity Proteins (Sp) and Cancer.International journal of molecular sciences · 2023Review
- Targeting HSF1 for cancer treatment: mechanisms and inhibitor development.Theranostics · 2023Review
- O-GlcNAcylation: an important post-translational modification and a potential therapeutic target for cancer therapy.Molecular medicine (Cambridge, Mass.) · 2022Review
- Altered glycosylation in pancreatic cancer and beyond.The Journal of experimental medicine · 2022Review
- The therapeutic potential of natural products for treating pancreatic cancer.Frontiers in pharmacology · 2022Review
- The Beginner's Guide toFrontiers in immunology · 2022Review
- O-GlcNAcylation and O-GlcNAc Cycling Regulate Gene Transcription: Emerging Roles in Cancer.Cancers · 2021Review
- Curcumin suppresses the proliferation of oral squamous cell carcinoma through a specificity protein 1/nuclear factor-κB-dependent pathway.Experimental and therapeutic medicine · 2021Article
- Proteomic profiling and genome-wide mapping of O-GlcNAc chromatin-associated proteins reveal an O-GlcNAc-regulated genotoxic stress response.Nature communications · 2020Article
- Enhanced Photothermal Therapy through the In Situ Activation of a Temperature and Redox Dual-Sensitive Nanoreservoir of Triptolide.Small (Weinheim an der Bergstrasse, Germany) · 2020Article
- Targeting tumor-intrinsic hexosamine biosynthesis sensitizes pancreatic cancer to anti-PD1 therapy.The Journal of clinical investigation · 2020Article
- Integrated network pharmacology and targeted metabolomics to reveal the mechanism of nephrotoxicity of triptolide.Toxicology research · 2019Article
- O-GlcNAc transferase suppresses necroptosis and liver fibrosis.JCI insight · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Pancreatic cancer, the fourth most prevalent cancer-related cause of death in the United States, is a disease with a dismal survival rate of 5% 5 years after diagnosis. One of the survival proteins responsible for its extraordinary ability to evade cell death is HSP70. A naturally derived compound, triptolide, and its water-soluble prodrug, Minnelide, down-regulate the expression of this protein in pancreatic cancer cells, thereby causing cell death. However, the mechanism of action of triptolide has not been elucidated. Our study shows that triptolide-induced down-regulation of HSP70 expression is associated with a decrease in glycosylation of the transcription factor Sp1. We further show that triptolide inhibits glycosylation of Sp1, inhibiting the hexosamine biosynthesis pathway, particularly the enzyme O-GlcNAc transferase. Inhibition of O-GlcNAc transferase prevents nuclear localization of Sp1 and affects its DNA binding activity. This in turn down-regulates prosurvival pathways like NF-κB, leading to inhibition of HSF1 and HSP70 and eventually to cell death. In this study, we evaluated the mechanism by which triptolide affects glycosylation of Sp1, which in turn affects downstream pathways controlling survival of pancreatic cancer cells.
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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.