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LASP1 in Cellular Signaling and Gene Expression: More than Just a Cytoskeletal Regulator

LIM and SH3 protein 1 was originally identified as a structural cytoskeletal protein with scaffolding function. However, recent data suggest additional roles in cell signaling and gene expression, especially in tumor cells. These novel functions are primarily regulated by the site-specific phosphory...

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Detalles Bibliográficos
Autores principales: Butt, Elke, Howard, Cory M., Raman, Dayanidhi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9741313/
https://www.ncbi.nlm.nih.gov/pubmed/36497077
http://dx.doi.org/10.3390/cells11233817
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author Butt, Elke
Howard, Cory M.
Raman, Dayanidhi
author_facet Butt, Elke
Howard, Cory M.
Raman, Dayanidhi
author_sort Butt, Elke
collection PubMed
description LIM and SH3 protein 1 was originally identified as a structural cytoskeletal protein with scaffolding function. However, recent data suggest additional roles in cell signaling and gene expression, especially in tumor cells. These novel functions are primarily regulated by the site-specific phosphorylation of LASP1. This review will focus on specific phosphorylation-dependent interaction between LASP1 and cellular proteins that orchestrate primary tumor progression and metastasis. More specifically, we will describe the role of LASP1 in chemokine receptor, and PI3K/AKT signaling. We outline the nuclear role for LASP1 in terms of epigenetics and transcriptional regulation and modulation of oncogenic mRNA translation. Finally, newly identified roles for the cytoskeletal function of LASP1 next to its known canonical F-actin binding properties are included.
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spelling pubmed-97413132022-12-11 LASP1 in Cellular Signaling and Gene Expression: More than Just a Cytoskeletal Regulator Butt, Elke Howard, Cory M. Raman, Dayanidhi Cells Review LIM and SH3 protein 1 was originally identified as a structural cytoskeletal protein with scaffolding function. However, recent data suggest additional roles in cell signaling and gene expression, especially in tumor cells. These novel functions are primarily regulated by the site-specific phosphorylation of LASP1. This review will focus on specific phosphorylation-dependent interaction between LASP1 and cellular proteins that orchestrate primary tumor progression and metastasis. More specifically, we will describe the role of LASP1 in chemokine receptor, and PI3K/AKT signaling. We outline the nuclear role for LASP1 in terms of epigenetics and transcriptional regulation and modulation of oncogenic mRNA translation. Finally, newly identified roles for the cytoskeletal function of LASP1 next to its known canonical F-actin binding properties are included. MDPI 2022-11-29 /pmc/articles/PMC9741313/ /pubmed/36497077 http://dx.doi.org/10.3390/cells11233817 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Butt, Elke
Howard, Cory M.
Raman, Dayanidhi
LASP1 in Cellular Signaling and Gene Expression: More than Just a Cytoskeletal Regulator
title LASP1 in Cellular Signaling and Gene Expression: More than Just a Cytoskeletal Regulator
title_full LASP1 in Cellular Signaling and Gene Expression: More than Just a Cytoskeletal Regulator
title_fullStr LASP1 in Cellular Signaling and Gene Expression: More than Just a Cytoskeletal Regulator
title_full_unstemmed LASP1 in Cellular Signaling and Gene Expression: More than Just a Cytoskeletal Regulator
title_short LASP1 in Cellular Signaling and Gene Expression: More than Just a Cytoskeletal Regulator
title_sort lasp1 in cellular signaling and gene expression: more than just a cytoskeletal regulator
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9741313/
https://www.ncbi.nlm.nih.gov/pubmed/36497077
http://dx.doi.org/10.3390/cells11233817
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