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Roles of ERK, PI3 kinase, and PLC-γ pathways induced by overexpression of translationally controlled tumor protein in HeLa cells
- Roles of ERK, PI3 kinase, and PLC-γ pathways induced by overexpression of translationally controlled tumor protein in HeLa cells
- Kim M.; Jung J.; Lee K.
- Ewha Authors
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- Archives of Biochemistry and Biophysics
- Archives of Biochemistry and Biophysics vol. 485, no. 1, pp. 82 - 87
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- We reported previously that translationally controlled tumor protein (TCTP) is a cytoplasmic repressor of Na,K-ATPase in HeLa cells. In the current study, we showed that TCTP overexpression using adenovirus as vehicle, induced partial inhibition of Na,K-ATPase; phosphorylation of EGFR tyrosine residues 845, 992, 1068, and 1148; activation of Ras/Raf/ERK pathway; activation of PI3K/Akt pathway; and phosphorylation of PLC-γ in HeLa cells. Specific inhibition of PI3K/Akt pathway in contrast to the inhibition of ERK, significantly decreased TCTP overexpression-induced survival signal. Inhibition of PLC-γ pathway significantly decreased TCTP overexpression-induced cell migration but inhibition of ERK had less effect. These results suggest that TCTP plays a key physiological role in cell survival through Akt pathway and migration through PLC-γ pathway. © 2009 Elsevier Inc. All rights reserved.
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