RapamycinFungusV1, Main, Exploration, bibRecord, 001740

Activation of the PTEN/mTOR/STAT3 pathway in breast cancer stem-like cells is required for viability and maintenance.

Identifieur interne : 001740 ( Main/Exploration ); précédent : 001739; suivant : 001741

Activation of the PTEN/mTOR/STAT3 pathway in breast cancer stem-like cells is required for viability and maintenance.

Auteurs : Jiangbing Zhou [États-Unis] ; Julia Wulfkuhle ; Hao Zhang ; Peihua Gu ; Yanqin Yang ; Jianghong Deng ; Joseph B. Margolick ; Lance A. Liotta ; Emanuel Petricoin ; Ying Zhang

Source :

Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 2007.

RBID : pubmed:17911267

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Breast Neoplasms (genetics), Breast Neoplasms (metabolism), Breast Neoplasms (pathology), Cell Cycle (MeSH), Cell Line, Tumor (MeSH), Cell Survival (MeSH), Female (MeSH), Humans (MeSH), Mice (MeSH), Mice, Nude (MeSH), Models, Biological (MeSH), Neoplasm Transplantation (MeSH), Neoplastic Stem Cells (metabolism), Neoplastic Stem Cells (pathology), Oligonucleotide Array Sequence Analysis (MeSH), PTEN Phosphohydrolase (metabolism), Protein Kinases (deficiency), Protein Kinases (genetics), Protein Kinases (metabolism), STAT3 Transcription Factor (deficiency), STAT3 Transcription Factor (genetics), STAT3 Transcription Factor (metabolism), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (MeSH).
MESH :
- chemical , deficiency : Protein Kinases, STAT3 Transcription Factor.
- chemical , genetics : Protein Kinases, STAT3 Transcription Factor.
- chemical , metabolism : PTEN Phosphohydrolase, Protein Kinases, STAT3 Transcription Factor.
- genetics : Breast Neoplasms.
- metabolism : Breast Neoplasms, Neoplastic Stem Cells.
- pathology : Breast Neoplasms, Neoplastic Stem Cells.
- Animals, Cell Cycle, Cell Line, Tumor, Cell Survival, Female, Humans, Mice, Mice, Nude, Models, Biological, Neoplasm Transplantation, Oligonucleotide Array Sequence Analysis, Signal Transduction, TOR Serine-Threonine Kinases.

Abstract

Side-population (SP) cells within cancers and cell lines are rare cell populations known to enrich cancer stem-like cells. In this study, we characterized SP cells from the human breast cancer cell line MCF7 as a model for cancer stem-like cells. Compared with non-SP cells, MCF7 SP cells had higher colony-formation ability in vitro and greater tumorigenicity in vivo, suggesting that MCF7 SP cells enrich cancer stem-like cells. cDNA microarray analysis of the SP cells indicated higher expression of ATP-binding cassette transporters and genes involved in quiescence, which were confirmed by quantitative RT-PCR and flow cytometry cell cycle analysis. To identify signal pathways important for cancer stem-like cells, we analyzed cDNA microarray data and identified nine pathways that were altered in the SP cells. To analyze the protein signaling networks, we used reverse-phase signaling pathway protein microarray technology and identified three signaling proteins that are significantly different between MCF7 SP and non-SP cells. Notably, signaling of phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin (mTOR), signal transduction and activator of transcription (STAT3), and phosphatase and tensin homolog (PTEN) was confirmed to be critical for MCF7 SP cell survival and proliferation by pathway specific inhibitors, selected gene knockdown, and in vivo tumorigenicity assay. The STAT3 pathway was found to be positively regulated by mTOR signaling, whereas PTEN served as a negative regulator of both STAT3 and mTOR signaling. This study suggests the existence of prosurvival signaling pathways critical for cancer stem-like cell maintenance, which could be selectively targeted for inhibiting cancer stem-like cells for improved treatment.

DOI: 10.1073/pnas.0702596104
PubMed: 17911267
PubMed Central: PMC2042178

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<author><name sortKey="Zhang, Hao" sort="Zhang, Hao" uniqKey="Zhang H" first="Hao" last="Zhang">Hao Zhang</name>
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<author><name sortKey="Gu, Peihua" sort="Gu, Peihua" uniqKey="Gu P" first="Peihua" last="Gu">Peihua Gu</name>
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<author><name sortKey="Yang, Yanqin" sort="Yang, Yanqin" uniqKey="Yang Y" first="Yanqin" last="Yang">Yanqin Yang</name>
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<author><name sortKey="Deng, Jianghong" sort="Deng, Jianghong" uniqKey="Deng J" first="Jianghong" last="Deng">Jianghong Deng</name>
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<term>Breast Neoplasms (genetics)</term>
<term>Breast Neoplasms (metabolism)</term>
<term>Breast Neoplasms (pathology)</term>
<term>Cell Cycle (MeSH)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Cell Survival (MeSH)</term>
<term>Female (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Nude (MeSH)</term>
<term>Models, Biological (MeSH)</term>
<term>Neoplasm Transplantation (MeSH)</term>
<term>Neoplastic Stem Cells (metabolism)</term>
<term>Neoplastic Stem Cells (pathology)</term>
<term>Oligonucleotide Array Sequence Analysis (MeSH)</term>
<term>PTEN Phosphohydrolase (metabolism)</term>
<term>Protein Kinases (deficiency)</term>
<term>Protein Kinases (genetics)</term>
<term>Protein Kinases (metabolism)</term>
<term>STAT3 Transcription Factor (deficiency)</term>
<term>STAT3 Transcription Factor (genetics)</term>
<term>STAT3 Transcription Factor (metabolism)</term>
<term>Signal Transduction (MeSH)</term>
<term>TOR Serine-Threonine Kinases (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Cellules souches tumorales (anatomopathologie)</term>
<term>Cellules souches tumorales (métabolisme)</term>
<term>Cycle cellulaire (MeSH)</term>
<term>Facteur de transcription STAT-3 (déficit)</term>
<term>Facteur de transcription STAT-3 (génétique)</term>
<term>Facteur de transcription STAT-3 (métabolisme)</term>
<term>Femelle (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Modèles biologiques (MeSH)</term>
<term>Phosphohydrolase PTEN (métabolisme)</term>
<term>Protein kinases (déficit)</term>
<term>Protein kinases (génétique)</term>
<term>Protein kinases (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris nude (MeSH)</term>
<term>Survie cellulaire (MeSH)</term>
<term>Séquençage par oligonucléotides en batterie (MeSH)</term>
<term>Sérine-thréonine kinases TOR (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
<term>Transplantation tumorale (MeSH)</term>
<term>Tumeurs du sein (anatomopathologie)</term>
<term>Tumeurs du sein (génétique)</term>
<term>Tumeurs du sein (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Protein Kinases</term>
<term>STAT3 Transcription Factor</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Protein Kinases</term>
<term>STAT3 Transcription Factor</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>PTEN Phosphohydrolase</term>
<term>Protein Kinases</term>
<term>STAT3 Transcription Factor</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cellules souches tumorales</term>
<term>Tumeurs du sein</term>
</keywords>
<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Facteur de transcription STAT-3</term>
<term>Protein kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Breast Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur de transcription STAT-3</term>
<term>Protein kinases</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>Facteur de transcription STAT-3</term>
<term>Phosphohydrolase PTEN</term>
<term>Protein kinases</term>
<term>Tumeurs du sein</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Breast Neoplasms</term>
<term>Neoplastic Stem Cells</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Cycle</term>
<term>Cell Line, Tumor</term>
<term>Cell Survival</term>
<term>Female</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Nude</term>
<term>Models, Biological</term>
<term>Neoplasm Transplantation</term>
<term>Oligonucleotide Array Sequence Analysis</term>
<term>Signal Transduction</term>
<term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cycle cellulaire</term>
<term>Femelle</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Modèles biologiques</term>
<term>Souris</term>
<term>Souris nude</term>
<term>Survie cellulaire</term>
<term>Séquençage par oligonucléotides en batterie</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Transduction du signal</term>
<term>Transplantation tumorale</term>
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<front><div type="abstract" xml:lang="en">Side-population (SP) cells within cancers and cell lines are rare cell populations known to enrich cancer stem-like cells. In this study, we characterized SP cells from the human breast cancer cell line MCF7 as a model for cancer stem-like cells. Compared with non-SP cells, MCF7 SP cells had higher colony-formation ability in vitro and greater tumorigenicity in vivo, suggesting that MCF7 SP cells enrich cancer stem-like cells. cDNA microarray analysis of the SP cells indicated higher expression of ATP-binding cassette transporters and genes involved in quiescence, which were confirmed by quantitative RT-PCR and flow cytometry cell cycle analysis. To identify signal pathways important for cancer stem-like cells, we analyzed cDNA microarray data and identified nine pathways that were altered in the SP cells. To analyze the protein signaling networks, we used reverse-phase signaling pathway protein microarray technology and identified three signaling proteins that are significantly different between MCF7 SP and non-SP cells. Notably, signaling of phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin (mTOR), signal transduction and activator of transcription (STAT3), and phosphatase and tensin homolog (PTEN) was confirmed to be critical for MCF7 SP cell survival and proliferation by pathway specific inhibitors, selected gene knockdown, and in vivo tumorigenicity assay. The STAT3 pathway was found to be positively regulated by mTOR signaling, whereas PTEN served as a negative regulator of both STAT3 and mTOR signaling. This study suggests the existence of prosurvival signaling pathways critical for cancer stem-like cell maintenance, which could be selectively targeted for inhibiting cancer stem-like cells for improved treatment.</div>
</front>
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<Title>Proceedings of the National Academy of Sciences of the United States of America</Title>
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<ArticleTitle>Activation of the PTEN/mTOR/STAT3 pathway in breast cancer stem-like cells is required for viability and maintenance.</ArticleTitle>
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<Abstract><AbstractText>Side-population (SP) cells within cancers and cell lines are rare cell populations known to enrich cancer stem-like cells. In this study, we characterized SP cells from the human breast cancer cell line MCF7 as a model for cancer stem-like cells. Compared with non-SP cells, MCF7 SP cells had higher colony-formation ability in vitro and greater tumorigenicity in vivo, suggesting that MCF7 SP cells enrich cancer stem-like cells. cDNA microarray analysis of the SP cells indicated higher expression of ATP-binding cassette transporters and genes involved in quiescence, which were confirmed by quantitative RT-PCR and flow cytometry cell cycle analysis. To identify signal pathways important for cancer stem-like cells, we analyzed cDNA microarray data and identified nine pathways that were altered in the SP cells. To analyze the protein signaling networks, we used reverse-phase signaling pathway protein microarray technology and identified three signaling proteins that are significantly different between MCF7 SP and non-SP cells. Notably, signaling of phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin (mTOR), signal transduction and activator of transcription (STAT3), and phosphatase and tensin homolog (PTEN) was confirmed to be critical for MCF7 SP cell survival and proliferation by pathway specific inhibitors, selected gene knockdown, and in vivo tumorigenicity assay. The STAT3 pathway was found to be positively regulated by mTOR signaling, whereas PTEN served as a negative regulator of both STAT3 and mTOR signaling. This study suggests the existence of prosurvival signaling pathways critical for cancer stem-like cell maintenance, which could be selectively targeted for inhibiting cancer stem-like cells for improved treatment.</AbstractText>
</Abstract>
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<ForeName>Jiangbing</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, The Johns Hopkins University, Baltimore, MD 21205, USA.</Affiliation>
</AffiliationInfo>
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<ForeName>Julia</ForeName>
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<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Hao</ForeName>
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<Author ValidYN="Y"><LastName>Gu</LastName>
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<Author ValidYN="Y"><LastName>Yang</LastName>
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<Author ValidYN="Y"><LastName>Deng</LastName>
<ForeName>Jianghong</ForeName>
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<ForeName>Joseph B</ForeName>
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<ForeName>Lance A</ForeName>
<Initials>LA</Initials>
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<Author ValidYN="Y"><LastName>Petricoin</LastName>
<ForeName>Emanuel</ForeName>
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<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Ying</ForeName>
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<Acronym>AI</Acronym>
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<CommentsCorrectionsList><CommentsCorrections RefType="ErratumIn"><RefSource>Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19655</RefSource>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
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<MeshHeading><DescriptorName UI="D001943" MajorTopicYN="N">Breast Neoplasms</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
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<MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName>
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<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008819" MajorTopicYN="N">Mice, Nude</DescriptorName>
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<MeshHeading><DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName>
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<MeshHeading><DescriptorName UI="D009368" MajorTopicYN="N">Neoplasm Transplantation</DescriptorName>
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<MeshHeading><DescriptorName UI="D014411" MajorTopicYN="N">Neoplastic Stem Cells</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
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<MeshHeading><DescriptorName UI="D020411" MajorTopicYN="N">Oligonucleotide Array Sequence Analysis</DescriptorName>
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<MeshHeading><DescriptorName UI="D051059" MajorTopicYN="N">PTEN Phosphohydrolase</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D011494" MajorTopicYN="N">Protein Kinases</DescriptorName>
<QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
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<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName>
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<Month>10</Month>
<Day>4</Day>
<Hour>9</Hour>
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Activation of the PTEN/mTOR/STAT3 pathway in breast cancer stem-like cells is required for viability and maintenance.

Activation of the PTEN/mTOR/STAT3 pathway in breast cancer stem-like cells is required for viability and maintenance.

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