ArticleOncotarget2015
Tauroursodeoxycholic acid dampens oncogenic apoptosis induced by endoplasmic reticulum stress during hepatocarcinogen exposure.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 45 citations in OpenAlex.
- Inhibiting endoplasmic reticulum stress and unfolded protein response: an effective strategy for chemoprevention of hepatocarcinogenesis.Molecular and cellular biochemistry · 2026Article
- Anti-inflammatory effects of taurocholic acid and tauroursodeoxycholic acid from rainbow trout spleen extract via NF-κB suppression.Scientific reports · 2026Article
- Combination treatment with epibrassinolide overcomes tamoxifen resistance in breast cancer cells via endoplasmic reticulum stress induction.Molecular biology reports · 2025Article
- The Roles and Clinical Significance of Major Hepatic-Derived Metabolites in Hepatocellular Carcinoma.Journal of gastroenterology and hepatology · 2025Review
- ER stress and/or ER-phagy in drug resistance? Three coincidences are proof.Cell communication and signaling : CCS · 2025Review
- Carcinogenic and anticancer activities of microbiota-derived secondary bile acids.Frontiers in oncology · 2025Review
- Bile Acids and Liver Cancer: Molecular Mechanism and Therapeutic Prospects.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Crosstalk between metabolism and cell death in tumorigenesis.Molecular cancer · 2024Review
- The anticancer activity of bile acids in drug discovery and development.Frontiers in pharmacology · 2024Review
- A novel maladaptive unfolded protein response as a mechanism for small bowel resection-induced liver injury.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- Mechanism of Bile Acid-Induced Programmed Cell Death and Drug Discovery against Cancer: A Review.International journal of molecular sciences · 2022Review
- Repair effect of the poly (D,L-lactic acid) nanoparticle containing tauroursodeoxycholic acid-eluting stents on endothelial injury after stent implantation.Frontiers in cardiovascular medicine · 2022Article
- Bile acids regulate intestinal antigen presentation and reduce graft-versus-host disease without impairing the graft-versus-leukemia effect.Haematologica · 2021Article
- Bile Acids and Microbiota: Multifaceted and Versatile Regulators of the Liver-Gut Axis.International journal of molecular sciences · 2021Review
- Resolution of eicosanoid/cytokine storm prevents carcinogen and inflammation-initiated hepatocellular cancer progression.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Tauroursodeoxycholic acid mediates endoplasmic reticulum stress and autophagy in adrenocortical carcinoma cells.Oncology letters · 2019Article
- Review
- Endoplasmic reticulum stress and liver diseases.Liver research (Beijing, China) · 2019Article
- Article
- Tauroursodeoxycholic acid attenuates endoplasmic reticulum stress and protects the liver from chronic intermittent hypoxia induced injury.Experimental and therapeutic medicine · 2017Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is characterized by the accumulation of unfolded proteins in the endoplasmic reticulum (ER), which activates the unfolded protein response (UPR). However, the role of ER stress in tumor initiation and progression is controversial. To determine the impact of ER stress, we applied tauroursodeoxycholic acid (TUDCA), a bile acid with chaperone properties. The effects of TUDCA were assessed using a diethylnitrosamine-induced mouse HCC model in preventive and therapeutic settings. Cell metabolic activity, proliferation and invasion were investigated in vitro. Tumor progression was assessed in the HepG2 xenograft model. Administration of TUDCA in the preventive setting reduced carcinogen-induced elevation of alanine and aspartate aminotransferase levels, apoptosis of hepatocytes and tumor burden. TUDCA also reduced eukaryotic initiation factor 2α (eIf2α) phosphorylation, C/EBP homologous protein expression and caspase-12 processing. Thus, TUDCA suppresses carcinogen-induced pro-apoptotic UPR. TUDCA alleviated hepatic inflammation by increasing NF-κB inhibitor IκBα. Furthermore, TUDCA altered the invasive phenotype and enhanced metabolic activity but not proliferation in HCC cells. TUDCA administration after tumor development did not alter orthotopic tumor or xenograft growth. Taken together, TUDCA attenuates hepatocarcinogenesis by suppressing carcinogen-induced ER stress-mediated cell death and inflammation without stimulating tumor progression. Therefore, this chemical chaperone could represent a novel chemopreventive agent.
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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.