Abstract
Translationally controlled tumor protein (TCTP) expression is suppressed during cancer cell reversion to a non-malignant phenotype. We identified a primary sequence of TCTP with homology to ADF/cofilin. We confirm that a synthetic peptide corresponding to this sequence binds specifically to actin and is displaced from actin by cofilin. TCTP peptide has higher affinity for G-actin than F-actin and does not block actin-filament depolymerization by cofilin. These results suggest that TCTP may channel active cofilin to F-actin, enhancing the cofilin-activity cycle in invasive tumor cells. Loss of TCTP may result in sequestration of active cofilin by a monomeric pool of actin.
Published by Elsevier B.V.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Actin Cytoskeleton / metabolism
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Actin Depolymerizing Factors / metabolism*
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Actins / chemistry
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Actins / metabolism*
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Amino Acid Sequence
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Animals
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Binding Sites
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Biomarkers, Tumor / chemistry*
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Biomarkers, Tumor / metabolism*
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Humans
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Mice
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Models, Molecular
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Molecular Sequence Data
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Peptide Fragments / chemistry
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Peptide Fragments / metabolism
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Protein Multimerization
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Protein Structure, Quaternary
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Rabbits
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Rats
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Substrate Specificity
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Tumor Protein, Translationally-Controlled 1
Substances
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Actin Depolymerizing Factors
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Actins
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Biomarkers, Tumor
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Peptide Fragments
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TPT1 protein, human
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Tpt1 protein, mouse
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Tpt1 protein, rat
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Tumor Protein, Translationally-Controlled 1