Cited by 99Bioactive Compounds and Antitumor AgentsCancer and biochemical researchMedicinal Plant Research

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Inducing the cell cycle arrest and apoptosis of oral KB carcinoma cells by hydroxychavicol: roles of glutathione and reactive oxygen species

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Chang, M C, Uang, B J, Wu, H L, Lee, J J, Hahn, L J, Jeng, J H·2002·British Journal of Pharmacology

Abstract

Hydroxychavicol (HC; 10 – 50 μ M), a betel leaf component, was found to suppress the 2% H 2 O 2‐induced lucigenin chemiluminescence for 53 – 75%. HC (0.02 – 2 μ M) was also able to trap superoxide radicals generated by a xanthine/xanthine oxidase system with 38 – 94% of inhibition. Hydroxyl radicals‐induced PUC18 plasmid DNA breaks was prevented by HC (1.6 – 16 μ M). A 24‐h exposure of KB cells to HC (0.5, 1 m M) resulted in 54 – 74% cell death as analysed by a 3‐(4,5‐dimethyl‐thiazol‐2‐yl)‐2,5‐diphenyl‐tetrazolium bromide (MTT) assay. HC (10, 50 μ M) further suppressed the growth of KB cells (15 and 76%, respectively). Long‐term colony formation of KB cells was inhibited by 51% with 10 μ M HC. Pretreatment of KB cells with 100 μ M HC inhibited the attachment of KB cells to type I collagen and fibronectin by 59 and 29%, respectively. Exposure of KB cells to 0.1 m M HC for 24 h resulted in cell cycle arrest at late S and G2/M phase. Increasing the HC concentration to 0.25 and 0.5 m M led to apoptosis as revealed by detection of sub‐G 0/G 1 peaks with a concomitant decrease in the number of cells residing in late S and G 2/M phase. Inducing the apoptosis of KB cells by HC was accompanied by marked depletion in reduced form of GSH (>0.2 m M) and the increasing of reactive oxygen species production (>0.1 m M) as analysed by CMF‐ and DCF‐single cell fluorescence flow cytometry. These results indicate that HC exerts antioxidant property at low concentration. HC also inhibits the growth, adhesion and cell cycle progression of KB cells, whereas its induction of KB cell apoptosis (HC>0.1 m M) was accompanied by cellular redox changes. British Journal of Pharmacology (2002) 135, 619–630; doi:10.1038/sj.bjp.0704492

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Metadata

Authors
Chang, M. C., Uang, B. J., Wu, H. L., Lee, J. J., Hahn, L. J., & Jeng, J. H.
Affiliations
  • Chang Gung University (TW)
  • National Tsing Hua University (TW)
  • National Taiwan University (TW)
Corresponding author
Jeng, J H
Venue
British Journal of Pharmacology
Publisher
Wiley
Published
2002-02
Volume
135
Issue
3
Pages
619-630
ISSN
  • 0007-1188 (ISSN-L)
  • 1476-5381
OpenAlex
W2038661189
Cited by
99
References
73
Citations by year
2026: 1 · 2025: 2 · 2024: 4 · 2023: 10 · 2022: 3 · 2021: 4 · 2020: 1 · 2019: 2 · 2018: 4 · 2017: 2 · 2016: 2 · 2015: 1 · 2014: 7 · 2013: 4 · 2012: 9
FWCI
5.33
Type
journal article
Language
en
Open access
Locations
  • British Journal of Pharmacology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Bioactive Compounds and Antitumor Agents
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
  • Life Sciences › Agricultural and Biological Sciences › Plant Science › Medicinal Plant Research
Keywords
hydroxychavicol, apoptosis, cell cycle arrest, glutathione, reactive oxygen species, antioxidant activity, superoxide radical scavenging, cell adhesion, G2/M cell cycle arrest
MeSH terms
Antineoplastic Agents, Areca, Cell Adhesion, Cell Cycle, Collagen, Dose-Response Relationship, Drug, Eugenol, Fibronectins, Glutathione, Growth Inhibitors, Humans, KB Cells, Anticarcinogenic Agents, Apoptosis, Reactive Oxygen Species, Oxidative Stress, Cell Size

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