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Plos One : Inhibition of Oxidative Stress-elicited Akt Activation Facilitates Pparγ Agonist-mediated Inhibition of Stem Cell Character and Tumor Growth of Liver Cancer Cells, Volume 8

By Tintut, Yin

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Book Id: WPLBN0003950691
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos One : Inhibition of Oxidative Stress-elicited Akt Activation Facilitates Pparγ Agonist-mediated Inhibition of Stem Cell Character and Tumor Growth of Liver Cancer Cells, Volume 8  
Author: Tintut, Yin
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection (Contemporary)
Historic
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Publisher: Plos

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Tintut, Y. (n.d.). Plos One : Inhibition of Oxidative Stress-elicited Akt Activation Facilitates Pparγ Agonist-mediated Inhibition of Stem Cell Character and Tumor Growth of Liver Cancer Cells, Volume 8. Retrieved from http://worldebookfair.com/


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Description : Emerging evidence suggests that tumor-initiating cells (TICs) are the most malignant cell subpopulation in tumors because of their resistance to chemotherapy or radiation treatment. Targeting TICs may be a key innovation for cancer treatment. In this study, we found that PPARc agonists inhibited the cancer stem cell-like phenotype and attenuated tumor growth of human hepatocellular carcinoma (HCC) cells. Reactive oxygen species (ROS) initiated by NOX2 upregulation were partially responsible for the inhibitory effects mediated by PPARc agonists. However, PPARc agonist-mediated ROS production significantly activated AKT, which in turn promoted TIC survival by limiting ROS generation. Inhibition of AKT, by either pharmacological inhibitors or AKT siRNA, significantly enhanced PPARc agonist-mediated inhibition of cell proliferation and stem cell-like properties in HCC cells. Importantly, in nude mice inoculated with HCC Huh7 cells, we demonstrated a synergistic inhibitory effect of the PPARc agonist rosiglitazone and the AKT inhibitor triciribine on tumor growth. In conclusion, we observed a negative feedback loop between oxidative stress and AKT hyperactivation in PPARc agonistmediated suppressive effects on HCCs. Combinatory application of an AKT inhibitor and a PPARc agonist may provide a new strategy for inhibition of stem cell-like properties in HCCs and treatment of liver cancer.

 

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