Abstract
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-gamma 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-gamma 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-gamma pathway.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenoviridae / genetics
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Animals
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Biomarkers, Tumor / biosynthesis
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Biomarkers, Tumor / genetics
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Biomarkers, Tumor / metabolism*
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ErbB Receptors / metabolism
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Extracellular Signal-Regulated MAP Kinases / metabolism*
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Gene Expression
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HeLa Cells
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Humans
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Phosphatidylinositol 3-Kinases / metabolism*
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Phospholipase C gamma / metabolism*
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Phosphorylation
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Proto-Oncogene Proteins c-akt / metabolism
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Proto-Oncogene Proteins c-raf / metabolism
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Signal Transduction*
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Sodium-Potassium-Exchanging ATPase / metabolism
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Tumor Protein, Translationally-Controlled 1
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ras Proteins / metabolism
Substances
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Biomarkers, Tumor
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TPT1 protein, human
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Tumor Protein, Translationally-Controlled 1
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ErbB Receptors
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Proto-Oncogene Proteins c-akt
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Proto-Oncogene Proteins c-raf
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Extracellular Signal-Regulated MAP Kinases
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Phospholipase C gamma
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ras Proteins
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Sodium-Potassium-Exchanging ATPase