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Downregulation of protein kinase CK2 activity induces age-related biomarkers in C. elegans

Title
Downregulation of protein kinase CK2 activity induces age-related biomarkers in C. elegans
Authors
Park, Jeong-HwanLee, Joo-HyunPark, Jeong-WooKim, Dong-YunHahm, Jeong-HoonNam, Hong GilBae, Young-Seuk
DGIST Authors
Nam, Hong Gil
Issue Date
2017-06-06
Citation
Oncotarget, 8(23), 36950-36963
Type
Article
Article Type
Article
Keywords
C. ElegansCaenorhabditis ElegansCellsCellular SenescenceCKIIDAF 16DAF 16DAF 16GerotargetHuman Colon CancerLifespanLongevityLongevityOxidative StressProtein Kinase CK2Protein Kinase CK2Regulation Mediated SenescenceTranscription Factor
ISSN
1949-2553
Abstract
Studies show that a decrease in protein kinase CK2 (CK2) activity is associated with cellular senescence. However, the role of CK2 in organism aging is still poorly understood. Here, we investigated whether protein kinase CK2 (CK2) modulated longevity in Caenorhabditis elegans. CK2 activity decreased with advancing age in the worms. Knockdown of kin-10 (the ortholog of CK2β) led to a short lifespan phenotype and induced age-related biomarkers, including retardation of locomotion, decreased pharyngeal pumping rate, increased lipofuscin accumulation, and reduced resistance to heat and oxidative stress. The long lifespan of age-1 and akt-1 mutants was significantly suppressed by kin-10 RNAi, suggesting that CK2 acts downstream of AGE- 1 and AKT-1. Kin-10 knockdown did not further shorten the short lifespan of daf-16 mutant worms but either decreased or increased the transcriptional activity of DAF-16 depending on the promoters of the target genes, indicating that CK2 is an upstream regulator of DAF-16 in C. elegans. Kin-10 knockdown increased production of reactive oxygen species (ROS) in the worms. Finally, the ROS scavenger N-acetyl-L-cysteine significantly counteracts the lifespan shortening and lipofuscin accumulation induced by kin-10 knockdown. Therefore, the present results suggest that age-dependent CK2 downregulation reduces longevity by associating with both ROS generation and the AGE-1-AKT-1-DAF-16 pathway in C. elegans. © Park et al.
URI
http://hdl.handle.net/20.500.11750/4155
DOI
10.18632/oncotarget.16939
Publisher
Impact Journals LLC
Related Researcher
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Collection:
New BiologyETC1. Journal Articles


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