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.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Cell Growth Processes / physiology
-
Cell Line, Tumor
-
Gene Expression Regulation, Neoplastic / physiology
-
Humans
-
Lung Neoplasms / genetics
-
Lung Neoplasms / metabolism*
-
Lung Neoplasms / pathology*
-
Neoplasm Invasiveness / genetics
-
Neoplasm Invasiveness / pathology
-
Oxidative Stress / genetics
-
Peroxiredoxin VI / genetics
-
Peroxiredoxin VI / metabolism*
-
Phosphatidylinositol 3-Kinases / metabolism*
-
Proto-Oncogene Proteins c-akt / metabolism
-
RNA, Small Interfering / genetics
-
Signal Transduction / genetics
-
Transgenes / genetics
-
Urokinase-Type Plasminogen Activator / biosynthesis*
-
Urokinase-Type Plasminogen Activator / genetics
-
p38 Mitogen-Activated Protein Kinases / metabolism
Substances
-
RNA, Small Interfering
-
PRDX6 protein, human
-
Peroxiredoxin VI
-
Phosphatidylinositol 3-Kinases
-
Proto-Oncogene Proteins c-akt
-
p38 Mitogen-Activated Protein Kinases
-
Urokinase-Type Plasminogen Activator