Roles of ERK, PI3 kinase, and PLC-γ pathways induced by overexpression of translationally controlled tumor protein in HeLa cells

Moonhee Kim, Jaehoon Jung, Kyunglim Lee

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

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 languageEnglish
Pages (from-to)82-87
Number of pages6
JournalArchives of Biochemistry and Biophysics
Volume485
Issue number1
DOIs
StatePublished - 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

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