C1-TEN is a negative regulator of the Akt/PKB signal transduction pathway and inhibits cell survival, proliferation, and migration Sassan Hafizi 1 , Filiz Ibraimi and Björn Dahlbäck Department of Clinical Chemistry, Lund University, Wallenberg Laboratory, University Hospital Malmö, Malmö, Sweden 1 Correspondence: Department of Clinical Chemistry, Lund University, Wallenberg Laboratory, University Hospital Malmö, SE-205 02 Malmö, Sweden. E-mail: sassan.hafizi@med.mas.lu.se <h3>SPECIFIC AIMS</h3> We have investigated the effects of overexpression of a novel intracellular molecule, C1 domain-containing phosphatase and TENsin homologue (C1-TEN), on the phenotypic and intracellular signal transduction properties of mammalian HEK293 cells. <h3>PRINCIPAL FINDINGS</h3> <h3>1. Stable overexpression of C1-TEN caused a profound alteration in cellular phenotype</h3> Mock transfected cells (M-293) showed an identical morphology to untransfected cells, whereas C1-TEN-transfected cells (C-293) possessed rounder and smoother cell bodies and slightly longer processes. C-293 cells displayed weaker fluorescent staining of filamentous actin. Therefore, C1-TEN overexpression clearly alters cytoskeletal architecture in HEK293 cells. <h3>2. Reduced proliferation and migration of C1-TEN-overexpressing cells</h3> Stable expression of C1-TEN markedly suppressed the growth rate of 293 cells as compared with mock transfection in response to serum over 5 days. Cells overexpressing the active site cysteine mutant C231S showed a fully restored rate of proliferation. C-293
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