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Overexpression of phosphoserine aminotransferase PSAT1 stimulates cell growth and increases chemoresistance of colon cancer cells

BACKGROUND: Colorectal cancer (CRC) is one of the most common causes of cancer death throughout the world. In this work our aim was to study the role of the phosphoserine aminotransferase PSAT1 in colorectal cancer development. RESULTS: We first observed that PSAT1 is overexpressed in colon tumors....

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Autores principales: Vié, Nadia, Copois, Virginie, Bascoul-Mollevi, Caroline, Denis, Vincent, Bec, Nicole, Robert, Bruno, Fraslon, Caroline, Conseiller, Emmanuel, Molina, Franck, Larroque, Christian, Martineau, Pierre, Del Rio, Maguy, Gongora, Céline
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2245978/
https://www.ncbi.nlm.nih.gov/pubmed/18221502
http://dx.doi.org/10.1186/1476-4598-7-14
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author Vié, Nadia
Copois, Virginie
Bascoul-Mollevi, Caroline
Denis, Vincent
Bec, Nicole
Robert, Bruno
Fraslon, Caroline
Conseiller, Emmanuel
Molina, Franck
Larroque, Christian
Martineau, Pierre
Del Rio, Maguy
Gongora, Céline
author_facet Vié, Nadia
Copois, Virginie
Bascoul-Mollevi, Caroline
Denis, Vincent
Bec, Nicole
Robert, Bruno
Fraslon, Caroline
Conseiller, Emmanuel
Molina, Franck
Larroque, Christian
Martineau, Pierre
Del Rio, Maguy
Gongora, Céline
author_sort Vié, Nadia
collection PubMed
description BACKGROUND: Colorectal cancer (CRC) is one of the most common causes of cancer death throughout the world. In this work our aim was to study the role of the phosphoserine aminotransferase PSAT1 in colorectal cancer development. RESULTS: We first observed that PSAT1 is overexpressed in colon tumors. In addition, we showed that after drug treatment, PSAT1 expression level in hepatic metastases increased in non responder and decreased in responder patients. In experiments using human cell lines, we showed that ectopic PSAT1 overexpression in colon carcinoma SW480 cell line resulted in an increase in its growth rate and survival. In addition, SW480-PSAT1 cells presented a higher tumorigenic potential than SW480 control cells in xenografted mice. Moreover, the SW480-PSAT1 cell line was more resistant to oxaliplatin treatment than the non-transfected SW480 cell line. This resistance resulted from a decrease in the apoptotic response and in the mitotic catastrophes induced by the drug treatment. CONCLUSION: These results show that an enzyme playing a role in the L-serine biosynthesis could be implicated in colon cancer progression and chemoresistance and indicate that PSAT1 represents a new interesting target for CRC therapy.
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spelling pubmed-22459782008-02-16 Overexpression of phosphoserine aminotransferase PSAT1 stimulates cell growth and increases chemoresistance of colon cancer cells Vié, Nadia Copois, Virginie Bascoul-Mollevi, Caroline Denis, Vincent Bec, Nicole Robert, Bruno Fraslon, Caroline Conseiller, Emmanuel Molina, Franck Larroque, Christian Martineau, Pierre Del Rio, Maguy Gongora, Céline Mol Cancer Research BACKGROUND: Colorectal cancer (CRC) is one of the most common causes of cancer death throughout the world. In this work our aim was to study the role of the phosphoserine aminotransferase PSAT1 in colorectal cancer development. RESULTS: We first observed that PSAT1 is overexpressed in colon tumors. In addition, we showed that after drug treatment, PSAT1 expression level in hepatic metastases increased in non responder and decreased in responder patients. In experiments using human cell lines, we showed that ectopic PSAT1 overexpression in colon carcinoma SW480 cell line resulted in an increase in its growth rate and survival. In addition, SW480-PSAT1 cells presented a higher tumorigenic potential than SW480 control cells in xenografted mice. Moreover, the SW480-PSAT1 cell line was more resistant to oxaliplatin treatment than the non-transfected SW480 cell line. This resistance resulted from a decrease in the apoptotic response and in the mitotic catastrophes induced by the drug treatment. CONCLUSION: These results show that an enzyme playing a role in the L-serine biosynthesis could be implicated in colon cancer progression and chemoresistance and indicate that PSAT1 represents a new interesting target for CRC therapy. BioMed Central 2008-01-25 /pmc/articles/PMC2245978/ /pubmed/18221502 http://dx.doi.org/10.1186/1476-4598-7-14 Text en Copyright © 2008 Vié et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Vié, Nadia
Copois, Virginie
Bascoul-Mollevi, Caroline
Denis, Vincent
Bec, Nicole
Robert, Bruno
Fraslon, Caroline
Conseiller, Emmanuel
Molina, Franck
Larroque, Christian
Martineau, Pierre
Del Rio, Maguy
Gongora, Céline
Overexpression of phosphoserine aminotransferase PSAT1 stimulates cell growth and increases chemoresistance of colon cancer cells
title Overexpression of phosphoserine aminotransferase PSAT1 stimulates cell growth and increases chemoresistance of colon cancer cells
title_full Overexpression of phosphoserine aminotransferase PSAT1 stimulates cell growth and increases chemoresistance of colon cancer cells
title_fullStr Overexpression of phosphoserine aminotransferase PSAT1 stimulates cell growth and increases chemoresistance of colon cancer cells
title_full_unstemmed Overexpression of phosphoserine aminotransferase PSAT1 stimulates cell growth and increases chemoresistance of colon cancer cells
title_short Overexpression of phosphoserine aminotransferase PSAT1 stimulates cell growth and increases chemoresistance of colon cancer cells
title_sort overexpression of phosphoserine aminotransferase psat1 stimulates cell growth and increases chemoresistance of colon cancer cells
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2245978/
https://www.ncbi.nlm.nih.gov/pubmed/18221502
http://dx.doi.org/10.1186/1476-4598-7-14
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