Dataset Information

Knockdown of 14-3-3? enhances radiosensitivity and radio-induced apoptosis in CD133(+) liver cancer stem cells.

ABSTRACT: 14-3-3? is related to many cancer survival cellular processes. In a previous study, we showed that silencing 14-3-3? decreases the resistance of hepatocellular carcinoma (HCC) to chemotherapy. In this study, we investigated whether silencing 14-3-3? affects the radioresistance of cancer stem-like cells (CSCs) in HCC. Knockdown of 14-3-3? decreased cell viability and the number of spheres by reducing radioresistance in CSCs after ?-irradiation (IR). Furthermore, the levels of pro-apoptotic proteins were upregulated in CSCs via silencing 14-3-3? after IR. These results suggest that 14-3-3? knockdown enhances radio-induced apoptosis by reducing radioresistance in liver CSCs.

SUBMITTER: Lee YK

PROVIDER: S-EPMC3944442 | biostudies-literature | 2014 Feb

REPOSITORIES: biostudies-literature

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Publications

Knockdown of 14-3-3ζ enhances radiosensitivity and radio-induced apoptosis in CD133(+) liver cancer stem cells.

Lee Young Ki YK Hur Wonhee W Lee Sung Won SW Hong Sung Woo SW Kim Sung Woo SW Choi Jung Eun JE Yoon Seung Kew SK

Experimental & molecular medicine 20140221

14-3-3ζ is related to many cancer survival cellular processes. In a previous study, we showed that silencing 14-3-3ζ decreases the resistance of hepatocellular carcinoma (HCC) to chemotherapy. In this study, we investigated whether silencing 14-3-3ζ affects the radioresistance of cancer stem-like cells (CSCs) in HCC. Knockdown of 14-3-3ζ decreased cell viability and the number of spheres by reducing radioresistance in CSCs after γ-irradiation (IR). Furthermore, the levels of pro-apoptotic protei ...[more]

PMID: 24556826

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Project description:ObjectiveMetabolic stress primes monocytes for accelerated chemokine-mediated adhesion, migration, and recruitment into vascular lesions by increasing actin remodeling. The mechanism linking metabolic stress to accelerated actin turnover and enhanced monocyte migration was not known. We tested the hypothesis that in metabolically primed monocytes, the acceleration of monocyte chemoattractant protein-1-induced chemotaxis is mediated by the hyperactivation of cofilin.Approach and resultsMetabolic priming was induced by exposing human THP-1 monocytes to diabetic conditions, that is, human native low-density lipoprotein plus high glucose concentrations. In healthy monocytes, monocyte chemoattractant protein-1 induced the phosphorylation and inactivation of cofilin. This response was completely blocked in metabolically primed monocytes but restored by overexpression of the thiol transferase, glutaredoxin 1. Cofilin kinase, LIM kinase 1, and cofilin phosphatase, Slingshot-1L, were not affected by metabolic stress. However, metabolic priming increased 3.8-fold the S-glutathionylation of the Slingshot-1L-binding protein 14-3-3ζ (zeta), resulting in its caspase-dependent degradation. Glutaredoxin 1 overexpression inhibited low-density lipoprotein plus high glucose-induced S-glutathionylation and degradation of 14-3-3ζ. The C25S mutant of 14-3-3ζ was resistant to both S-glutathionylation and degradation induced by low-density lipoprotein plus high glucose. Overexpression of the C25S mutant restored monocyte chemoattractant protein-1-induced cofilin phosphorylation and prevented accelerated migration of metabolically stressed monocytes, suggesting that loss of 14-3-3ζ increases the pool of free Slingshot-1L phosphatase, thereby preventing the phosphorylation and deactivation of cofilin in response to chemokine activation.ConclusionsBy preventing the inactivation of cofilin, metabolic stress-induced degradation of 14-3-3ζ promotes the conversion of blood monocytes into a hypermigratory, proatherogenic phenotype.

Dataset Information

Knockdown of 14-3-3? enhances radiosensitivity and radio-induced apoptosis in CD133(+) liver cancer stem cells.

Publications

Knockdown of 14-3-3ζ enhances radiosensitivity and radio-induced apoptosis in CD133(+) liver cancer stem cells.

Similar Datasets

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