National Tsing Hua University Institutional Repository:Activation of protein kinase Ca signaling prevents cytotoxicity and mutagenicity following lead acetate in CL3 human lung cancer cells
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    National Tsing Hua University Institutional Repository > 生命科學院  > 生命科學系 > 期刊論文 >  Activation of protein kinase Ca signaling prevents cytotoxicity and mutagenicity following lead acetate in CL3 human lung cancer cells


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    題名: Activation of protein kinase Ca signaling prevents cytotoxicity and mutagenicity following lead acetate in CL3 human lung cancer cells
    作者: Wang CY;Lin YW;YangJL
    教師: 楊嘉鈴
    日期: 2008
    出版者: Elsevier
    關聯: Toxicology,Elsevier,Volume 250,Issue 1,2008,Pages 55-61
    關鍵詞: Cancer
    Malignant tumor
    Lung disease
    Bronchus disease
    Respiratory disease
    Heavy metal
    摘要: Protein kinase C (PKC) family of serine/threonine protein kinases is sensitive signaling transducers in response to lead acetate (Pb) that could transmit phosphorylation cascade for proliferation and de-differentiation of neural cells. However, little is known as to the impact of PKC on Pb genotoxicity. Here we investigate whether Pb activates the conventional/classical subfamily of PKC (cPKC) signaling to affect cytotoxicity and mutagenicity in CL3 human non-small-cell lung adenocarcinoma cells. Pb specifically promoted membrane localization of the a isoform of PKC in CL3 cells. Pb also elicited Raf-1 activation as measured by the induction of phospho-Raf-1S338 and the dissociation from the Raf-1 kinase inhibitor protein. Inhibition of cPKC activity using Gö6976 or depletion of PKCα by introducing specific small interfering RNA blocked the induction of phospho-Raf-1S338, phospho-MKK1/2 and phospho-ERK1/2 in cells exposed to Pb. Intriguingly, declining PKCa enhanced the Pb cytotoxicity and revealed the Pb mutagenicity at the hprt gene. The results suggest that PKCa is obligatory for activation of the Raf-1-MKK1/2-ERK1/2 signaling module and plays a defensive role against cytotoxicity and mutagenicity following Pb exposure. Results obtained in this study also support our previous report showing that ERK1/2 activity is involved in preventing Pb genotoxicity.
    URI: http://cat.inist.fr/?aModele=afficheN&cpsidt=20573119
    http://www.elsevier.com/
    http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/49405
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