Thus, knockdown of p53 and overexpression

of p65 abrogate

Thus, knockdown of p53 and overexpression

of p65 abrogated the effect of NAC on PDK1 expression and cell proliferation highlighted the critical role of p53 and p65 in this process. Conclusion In summary, our results show that NAC inhibits PDK1 expression through PPARα-mediated this website induction of p53 and reduction of p65 protein expression. Activation of PPARα enhances this process. This leads to inhibit NSCLC cell growth. This study unveils a novel mechanism by which NAC in combination with PPARα ligand inhibits growth of human lung carcinoma cells. Acknowledgments We are grateful to Dr. Michalik (University of Lausanne in Switzerland) for providing SB202190 the PDK1 promoter construct, Dr. Jean J. Zhao (Dana Farber Cancer Institute, USA) for providing PDK1 expression vectors, Dr. Warner C. Greene (Duke University Medical Center, USA) for p65 expression vectors. This work was in part supported by the Special Science and Technology Join fund from Guangdong Provincial Department of Science and Technology-Guangdong Academy of Traditional Chinese Medicine (2012A032500011) and a grant from the National Nature Scientific Foundation of China (81272614). References 1. Siegel R, Naishadham D, Jemal A: Cancer statistics, 2013. CA Cancer J Clin 2013,63(1):11–30.PubMedCrossRef

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