ArticlePloS one2013
Antioxidant N-acetylcysteine attenuates hepatocarcinogenesis by inhibiting ROS/ER stress in TLR2 deficient mouse.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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
28 citing papers in PubMed, 58 citations in OpenAlex.
- Regulation of immune tolerance in hepatocellular carcinoma by liver diseases: a review.Infectious agents and cancer · 2026Review
- A Review of ARID1A's Role in Breast Cancer Progression: Context-Dependent Mechanisms and Therapeutic Implications.Cancers · 2025Review
- Article
- A new opportunity for N-acetylcysteine. An outline of its classic antioxidant effects and its pharmacological potential as an epigenetic modulator in liver diseases treatment.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Resveratrol and N-acetylcystein reduce hepatic steatosis but enhance initiation and progression of hepatocellular carcinoma by inhibiting GST-pi-MAPK axis in mice.Frontiers in pharmacology · 2025Article
- Protective effect of N-acetylcysteine against hepatocellular carcinoma in hepatitis B virus carriers.American journal of cancer research · 2024Article
- Does each Component of Reactive Oxygen Species have a Dual Role in the Tumor Microenvironment?Current medicinal chemistry · 2024Review
- Article
- CO-Releasing Molecule-2 Prevents Acute Kidney Injury through Suppression of ROS-Fyn-ER Stress Signaling in Mouse Model.Oxidative medicine and cellular longevity · 2021Article
- Anticancer effect of caudatin in diethylnitrosamine‑induced hepatocarcinogenesis in rats.Molecular medicine reports · 2020Article
- Silica nanoparticles induce unfolded protein reaction mediated apoptosis in spermatocyte cells.Toxicology research · 2020Article
- Endoplasmic Reticulum (ER) Stress Inhibitor or Antioxidant Treatments during Micromanipulation Can Inhibit Both ER and Oxidative Stresses in Porcine SCNT Embryos.Development & reproduction · 2020Article
- Mitochondrial Dysfunction in the Transition from NASH to HCC.Metabolites · 2019Review
- L-lysine protects C2C12 myotubes and 3T3-L1 adipocytes against high glucose damages and stresses.PloS one · 2019Article
- The Endoplasmic Reticulum Stress Response in Neuroprogressive Diseases: Emerging Pathophysiological Role and Translational Implications.Molecular neurobiology · 2018Review
- Carbon monoxide releasing molecule-2 protects mice against acute kidney injury through inhibition of ER stress.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018Article
- Endoplasmic reticulum stress stimulates the release of extracellular vesicles carrying danger-associated molecular pattern (DAMP) molecules.Oncotarget · 2018Article
- Effects of urban coarse particles inhalation on oxidative and inflammatory parameters in the mouse lung and colon.Particle and fibre toxicology · 2017Article
- Arid1a Has Context-Dependent Oncogenic and Tumor Suppressor Functions in Liver Cancer.Cancer cell · 2017Article
- HCV-related liver and lymphoproliferative diseases: association with polymorphisms of IL28B and TLR2.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) remains one of the most deadly solid tumor malignancies worldwide. We recently find that the loss of toll-like receptor 2 (TLR2) activities promotes the diethylnitrosamine (DEN) induced hepatocellular carcinogenesis and tumor progression, which associates with an abundant accumulation of reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress. This finding suggests that the ROS/ER stress plays a role in TLR2 modulated carcinogenesis of HCC. To investigate the mechanism of TLR2 activity defending against hepatocarcinogenesis, the TLR2-deficient mice were treated with or without antioxidant N-acetylcysteine (NAC) before DEN administration. We found that pretreatment of these animals with NAC attenuated carcinogenesis and progression of HCC in the TLR2-deficient mice, declined ROS/ER stress, and alleviated the unfold protein response and inflammatory response in TLR2-deficient liver tissue. Moreover, the NAC treatment significantly reduced the enhanced aggregation of p62 and Mallory-Denk bodies in the DEN-induced HCC liver tissue, suggesting that NAC treatment improves the suppressive autophagic flux in the TLR2-deficient liver. These findings indicate that TLR2 activity defends against hepatocarcinogenesis through diminishing the accumulation of ROS and alleviating ER stress and unfold protein response mediated inflammatory response in the liver.
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