AustralieFrV1, Main, Curation, bibRecord, 002717

The p53 Isoform Δ133p53β Promotes Cancer Stem Cell Potential

Identifieur interne : 002717 ( Main/Curation ); précédent : 002716; suivant : 002718

The p53 Isoform Δ133p53β Promotes Cancer Stem Cell Potential

Auteurs : Nikola Arsic [France] ; Gilles Gadea [France] ; E. Louise Lagerqvist [France] ; Muriel Busson [France] ; Nathalie Cahuzac [France] ; Carsten Brock [France] ; Frederic Hollande [Australie] ; Veronique Gire [France] ; Julie Pannequin [France] ; Pierre Roux [France]

Source :

Stem Cell Reports [ 2213-6711 ] ; 2015.

RBID : PMC:4400643

Descripteurs français

KwdFr :
- Analyse de profil d'expression de gènes, Antinéoplasiques (pharmacologie), Antinéoplasiques (usage thérapeutique), Auto-renouvellement cellulaire (génétique), Cellules MCF-7, Cellules cancéreuses en culture, Cellules souches tumorales (métabolisme), Facteurs de transcription (génétique), Femelle, Humains, Isoformes d'ARN, Lignée cellulaire tumorale, Mouvement cellulaire (génétique), Protéine p53 suppresseur de tumeur (génétique), Protéine p53 suppresseur de tumeur (métabolisme), Régulation de l'expression des gènes tumoraux (), Sphéroïdes de cellules, Tumeurs du sein (génétique), Tumeurs du sein (métabolisme), Tumeurs du sein (traitement médicamenteux), Épissage alternatif.
MESH :
- génétique : Auto-renouvellement cellulaire, Facteurs de transcription, Mouvement cellulaire, Protéine p53 suppresseur de tumeur, Tumeurs du sein.
- métabolisme : Cellules souches tumorales, Protéine p53 suppresseur de tumeur, Tumeurs du sein.
- pharmacologie : Antinéoplasiques.
- traitement médicamenteux : Tumeurs du sein.
- usage thérapeutique : Antinéoplasiques.
- Analyse de profil d'expression de gènes, Cellules MCF-7, Cellules cancéreuses en culture, Femelle, Humains, Isoformes d'ARN, Lignée cellulaire tumorale, Régulation de l'expression des gènes tumoraux, Sphéroïdes de cellules, Épissage alternatif.

English descriptors

KwdEn :
- Alternative Splicing, Antineoplastic Agents (pharmacology), Antineoplastic Agents (therapeutic use), Breast Neoplasms (drug therapy), Breast Neoplasms (genetics), Breast Neoplasms (metabolism), Cell Line, Tumor, Cell Movement (genetics), Cell Self Renewal (genetics), Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic (drug effects), Humans, MCF-7 Cells, Neoplastic Stem Cells (metabolism), RNA Isoforms, Spheroids, Cellular, Transcription Factors (genetics), Tumor Cells, Cultured, Tumor Suppressor Protein p53 (genetics), Tumor Suppressor Protein p53 (metabolism).
MESH :
- chemical , genetics : Transcription Factors, Tumor Suppressor Protein p53.
- chemical , metabolism : Tumor Suppressor Protein p53.
- chemical , pharmacology : Antineoplastic Agents.
- chemical , therapeutic use : Antineoplastic Agents.
- drug effects : Gene Expression Regulation, Neoplastic.
- drug therapy : Breast Neoplasms.
- genetics : Breast Neoplasms, Cell Movement, Cell Self Renewal.
- metabolism : Breast Neoplasms, Neoplastic Stem Cells.
- Alternative Splicing, Cell Line, Tumor, Female, Gene Expression Profiling, Humans, MCF-7 Cells, RNA Isoforms, Spheroids, Cellular, Tumor Cells, Cultured.

Abstract

Summary

Cancer stem cells (CSC) are responsible for cancer chemoresistance and metastasis formation. Here we report that Δ133p53β, a TP53 splice variant, enhanced cancer cell stemness in MCF-7 breast cancer cells, while its depletion reduced it. Δ133p53β stimulated the expression of the key pluripotency factors SOX2, OCT3/4, and NANOG. Similarly, in highly metastatic breast cancer cells, aggressiveness was coupled with enhanced CSC potential and Δ133p53β expression. Like in MCF-7 cells, SOX2, OCT3/4, and NANOG expression were positively regulated by Δ133p53β in these cells. Finally, treatment of MCF-7 cells with etoposide, a cytotoxic anti-cancer drug, increased CSC formation and SOX2, OCT3/4, and NANOG expression via Δ133p53, thus potentially increasing the risk of cancer recurrence. Our findings show that Δ133p53β supports CSC potential. Moreover, they indicate that the TP53 gene, which is considered a major tumor suppressor gene, also acts as an oncogene via the Δ133p53β isoform.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4400643

DOI: 10.1016/j.stemcr.2015.02.001
PubMed: 25754205
PubMed Central: 4400643

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PMC:4400643

Le document en format XML

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<country xml:lang="fr">France</country>
<wicri:regionArea>Centre National de la Recherche Scientifique, UMR 5237, Centre de Recherche en Biochimie Macromoléculaire, Université Montpellier, 1919 route de Mende, 34293 Montpellier Cedex 5</wicri:regionArea>
<wicri:noRegion>34293 Montpellier Cedex 5</wicri:noRegion>
<wicri:noRegion>34293 Montpellier Cedex 5</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series><title level="j">Stem Cell Reports</title>
<idno type="eISSN">2213-6711</idno>
<imprint><date when="2015">2015</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alternative Splicing</term>
<term>Antineoplastic Agents (pharmacology)</term>
<term>Antineoplastic Agents (therapeutic use)</term>
<term>Breast Neoplasms (drug therapy)</term>
<term>Breast Neoplasms (genetics)</term>
<term>Breast Neoplasms (metabolism)</term>
<term>Cell Line, Tumor</term>
<term>Cell Movement (genetics)</term>
<term>Cell Self Renewal (genetics)</term>
<term>Female</term>
<term>Gene Expression Profiling</term>
<term>Gene Expression Regulation, Neoplastic (drug effects)</term>
<term>Humans</term>
<term>MCF-7 Cells</term>
<term>Neoplastic Stem Cells (metabolism)</term>
<term>RNA Isoforms</term>
<term>Spheroids, Cellular</term>
<term>Transcription Factors (genetics)</term>
<term>Tumor Cells, Cultured</term>
<term>Tumor Suppressor Protein p53 (genetics)</term>
<term>Tumor Suppressor Protein p53 (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term>
<term>Antinéoplasiques (pharmacologie)</term>
<term>Antinéoplasiques (usage thérapeutique)</term>
<term>Auto-renouvellement cellulaire (génétique)</term>
<term>Cellules MCF-7</term>
<term>Cellules cancéreuses en culture</term>
<term>Cellules souches tumorales (métabolisme)</term>
<term>Facteurs de transcription (génétique)</term>
<term>Femelle</term>
<term>Humains</term>
<term>Isoformes d'ARN</term>
<term>Lignée cellulaire tumorale</term>
<term>Mouvement cellulaire (génétique)</term>
<term>Protéine p53 suppresseur de tumeur (génétique)</term>
<term>Protéine p53 suppresseur de tumeur (métabolisme)</term>
<term>Régulation de l'expression des gènes tumoraux ()</term>
<term>Sphéroïdes de cellules</term>
<term>Tumeurs du sein (génétique)</term>
<term>Tumeurs du sein (métabolisme)</term>
<term>Tumeurs du sein (traitement médicamenteux)</term>
<term>Épissage alternatif</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Transcription Factors</term>
<term>Tumor Suppressor Protein p53</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Tumor Suppressor Protein p53</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antineoplastic Agents</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression Regulation, Neoplastic</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Breast Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Breast Neoplasms</term>
<term>Cell Movement</term>
<term>Cell Self Renewal</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Auto-renouvellement cellulaire</term>
<term>Facteurs de transcription</term>
<term>Mouvement cellulaire</term>
<term>Protéine p53 suppresseur de tumeur</term>
<term>Tumeurs du sein</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Breast Neoplasms</term>
<term>Neoplastic Stem Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules souches tumorales</term>
<term>Protéine p53 suppresseur de tumeur</term>
<term>Tumeurs du sein</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs du sein</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Antinéoplasiques</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Alternative Splicing</term>
<term>Cell Line, Tumor</term>
<term>Female</term>
<term>Gene Expression Profiling</term>
<term>Humans</term>
<term>MCF-7 Cells</term>
<term>RNA Isoforms</term>
<term>Spheroids, Cellular</term>
<term>Tumor Cells, Cultured</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term>
<term>Cellules MCF-7</term>
<term>Cellules cancéreuses en culture</term>
<term>Femelle</term>
<term>Humains</term>
<term>Isoformes d'ARN</term>
<term>Lignée cellulaire tumorale</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Sphéroïdes de cellules</term>
<term>Épissage alternatif</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><title>Summary</title>
<p>Cancer stem cells (CSC) are responsible for cancer chemoresistance and metastasis formation. Here we report that Δ133p53β, a <italic>TP53</italic>
 splice variant, enhanced cancer cell stemness in MCF-7 breast cancer cells, while its depletion reduced it. Δ133p53β stimulated the expression of the key pluripotency factors <italic>SOX2</italic>
, <italic>OCT3/4</italic>
, and <italic>NANOG</italic>
. Similarly, in highly metastatic breast cancer cells, aggressiveness was coupled with enhanced CSC potential and Δ133p53β expression. Like in MCF-7 cells, <italic>SOX2</italic>
, <italic>OCT3/4</italic>
, and <italic>NANOG</italic>
 expression were positively regulated by Δ133p53β in these cells. Finally, treatment of MCF-7 cells with etoposide, a cytotoxic anti-cancer drug, increased CSC formation and <italic>SOX2</italic>
, <italic>OCT3/4</italic>
, and <italic>NANOG</italic>
 expression via Δ133p53, thus potentially increasing the risk of cancer recurrence. Our findings show that Δ133p53β supports CSC potential. Moreover, they indicate that the <italic>TP53</italic>
 gene, which is considered a major tumor suppressor gene, also acts as an oncogene via the Δ133p53β isoform.</p>
</div>
</front>
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	Serveur d'exploration sur les relations entre la France et l'Australie
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Serveur d'exploration sur les relations entre la France et l'Australie

The p53 Isoform Δ133p53β Promotes Cancer Stem Cell Potential

The p53 Isoform Δ133p53β Promotes Cancer Stem Cell Potential

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