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-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.
Original language | English |
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Pages (from-to) | 82-87 |
Number of pages | 6 |
Journal | Archives of Biochemistry and Biophysics |
Volume | 485 |
Issue number | 1 |
DOIs | |
State | Published - 1 May 2009 |
Bibliographical note
Funding Information:This work was supported by the Korea Research Foundation Grant funded by the Korean Government (MOEHRD, Basic Research Promotion Fund), the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MOST) (R01-2007-000-20263-0), and the NCRC program of MOST/KOSEF (R15-2006-020) through the Center for Cell Signalling and Drug Discovery at Ewha Womans University.
Keywords
- EGFR
- ERK
- Na,K-ATPase
- Ouabain
- PI3K
- PLC-γ
- TCTP