Int Neurourol J.  2016 Sep;20(3):182-187. 10.5213/inj.1632718.359.

Controls of Nuclear Factor-Kappa B Signaling Activity by 5’-AMP-Activated Protein Kinase Activation With Examples in Human Bladder Cancer Cells

Affiliations
  • 1Department of Pharmacology, Hypoxia-Related Disease Research Center, Inha Research Institute for Medical Sciences, Inha University College of Medicine, Incheon, Korea. parkshin@inha.ac.kr
  • 2Department of Anesthesiology and Pain Medicine, Inha University College of Medicine, Incheon, Korea.

Abstract

Generally, both lipopolysaccharide (LPS)- and hypoxia-induced nuclear factor kappa B (NF-κB) effects are alleviated through differential posttranslational modification of NF-κB phosphorylation after pretreatment with 5'-AMP-activated protein kinase (AMPK) activators such as 5'-aminoimidazole-4-carboxamide ribonucleotide (AICAR) or the hypoglycemic agent metformin. We found that AICAR or metformin acts as a regulator of LPS/NF-κB-or hypoxia/NF-κB-mediated cyclooxygenase induction by an AMPK-dependent mechanism with interactions between p65-NF-κB phosphorylation and acetylation, including in a human bladder cancer cell line (T24). In summary, we highlighted the regulatory interactions of AMPK activity on NF-κB induction, particularly in posttranslational phosphorylation and acetylation of NF-κB under inflammatory conditions or hypoxia environment.

Keyword

NF-kappa B; AMP-Activated Protein Kinases; Lipopolysaccharides; Hypoxia

MeSH Terms

Acetylation
AMP-Activated Protein Kinases
Anoxia
Cell Line
Humans*
Lipopolysaccharides
Metformin
NF-kappa B
Phosphorylation
Prostaglandin-Endoperoxide Synthases
Protein Kinases*
Protein Processing, Post-Translational
Urinary Bladder Neoplasms*
Urinary Bladder*
AMP-Activated Protein Kinases
Lipopolysaccharides
Metformin
NF-kappa B
Prostaglandin-Endoperoxide Synthases
Protein Kinases
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