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http://dx.doi.org/10.1007/s10059-009-0152-6

Peroxiredoxin 6 Promotes Lung Cancer Cell Invasion by Inducing Urokinase-Type Plasminogen Activator via p38 Kinase, Phosphoinositide 3-Kinase, and Akt  

Lee, Seung Bum (Laboratory of Radiation Tumor Physiology, Korea Institute of Radiological and Medical Sciences)
Ho, Jin-Nyoung (Laboratory of Radiation Tumor Physiology, Korea Institute of Radiological and Medical Sciences)
Yoon, Sung Hwan (Laboratory of Radiation Tumor Physiology, Korea Institute of Radiological and Medical Sciences)
Kang, Ga Young (Laboratory of Radiation Tumor Physiology, Korea Institute of Radiological and Medical Sciences)
Hwang, Sang-Gu (Laboratory of Radiation Tumor Physiology, Korea Institute of Radiological and Medical Sciences)
Um, Hong-Duck (Laboratory of Radiation Tumor Physiology, Korea Institute of Radiological and Medical Sciences)
Publication Information
Molecules and Cells / v.28, no.6, 2009 , pp. 583-588 More about this Journal
Abstract
The peroxiredoxin family of peroxidase has six mammalian members (Prx 1-6). Considering their frequent up-regulation in cancer cells, Prxs may contribute to cancer cells' survival in face of oxidative stress. Here, we show that Prx 6 promotes the invasiveness of lung cancer cells, accompanied by an increase in the activity of phosphoinositide 3-kinase (PI3K), the phosphorylation of p38 kinase and Akt, and the protein levels of uPA. Functional studies reveal that these components support Prx 6-induced invasion in the sequence p38 kinase/PI3K, Akt, and uPA. The findings provide a new understanding of the action of Prx 6 in cancer.
Keywords
cancer; cell signaling; invasion; peroxiredoxin 6;
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Times Cited By KSCI : 1  (Citation Analysis)
Times Cited By Web Of Science : 6  (Related Records In Web of Science)
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