ArticleBioscience reports2017
Glibenclamide induces apoptosis by activating reactive oxygen species dependent JNK pathway in hepatocellular carcinoma cells.
Article in Bioscience reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Succinylation: novel molecular mechanisms and prospects for targeted therapy in liver diseases.Frontiers in molecular biosciences · 2026Review
- CPT1A-mediated MFF succinylation promotes stemness maintenance in ovarian cancer stem cells.Communications biology · 2025Article
- Mechanism and therapeutic potential of liver injury induced by cholesterol-associated proteins.Frontiers in pharmacology · 2025Review
- Glyburide Suppresses Inflammation-Related Colorectal Tumorigenesis Through Inhibition of NLRP3 Inflammasome.International journal of molecular sciences · 2024Article
- Implications of NLRP3 Suppression Using Glibenclamide and miR-223 against Colorectal Cancer.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Exploitation of ATP-sensitive potassium ion (KOncogene · 2023Article
- Mitochondrial supercomplex assembly regulates metabolic features and glutamine dependency in mammalian cells.Theranostics · 2023Article
- Prognostic roles of diabetes mellitus and hypertension in advanced hepatocellular carcinoma treated with sorafenib.PloS one · 2020Article
- Review
- Maduramicin induces apoptosis through ROS-PP5-JNK pathway in skeletal myoblast cells and muscle tissue.Toxicology · 2019Article
- Differentially expressed genes of HepG2 cells treated with gecko polypeptide mixture.Journal of Cancer · 2018Article
- Downregulation of LEF1 Impairs Myeloma Cell Growth Through Modulating CYLD/NF-κB Signaling.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glibenclamide (Gli) is a widely employed drug in the treatment of type 2 diabetes and many lines of evidence have described its anti-tumor effects in some neoplasms. The aim of the present study was to investigate the effect of Gli on apoptosis of human hepatocellular carcinoma (HCC) cells and to analyze the underlying pathway involved in this action. Two HCC cell lines, HepG-2 and Huh7 were used as the cell models. We found that Gli treatment significantly inhibited cell viability, induced a significant cell-cycle arrest in G
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