Translation control during prolonged mTORC1 inhibition mediated by 4E-BP3.
Identifieur interne : 000970 ( Main/Exploration ); précédent : 000969; suivant : 000971Translation control during prolonged mTORC1 inhibition mediated by 4E-BP3.
Auteurs : Yoshinori Tsukumo [Canada] ; Tommy Alain [Canada] ; Bruno D. Fonseca [Canada] ; Robert Nadon [Canada] ; Nahum Sonenberg [Canada]Source :
- Nature communications [ 2041-1723 ] ; 2016.
Descripteurs français
- KwdFr :
- Analyse de survie (MeSH), Animaux (MeSH), Antibiotiques antinéoplasiques (pharmacologie), Bases de données génétiques (MeSH), Biosynthèse des protéines (MeSH), Cellules HeLa (MeSH), Cellules HepG2 (MeSH), Cellules MCF-7 (MeSH), Facteurs d'initiation eucaryotes (génétique), Facteurs d'initiation eucaryotes (métabolisme), Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines (génétique), Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines (métabolisme), Femelle (MeSH), Humains (MeSH), Indoles (pharmacologie), Mâle (MeSH), Phosphoprotéines (génétique), Phosphoprotéines (métabolisme), Prolifération cellulaire (MeSH), Protéines adaptatrices de la transduction du signal (génétique), Protéines adaptatrices de la transduction du signal (métabolisme), Protéines de transport (génétique), Protéines de transport (métabolisme), Purines (pharmacologie), Régulation de l'expression des gènes tumoraux (MeSH), Sirolimus (pharmacologie), Souris (MeSH), Souris de lignée C57BL (MeSH), Systèmes CRISPR-Cas (MeSH), Sérine-thréonine kinases TOR (antagonistes et inhibiteurs), Sérine-thréonine kinases TOR (génétique), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (MeSH), Tumeurs du sein (anatomopathologie), Tumeurs du sein (génétique), Tumeurs du sein (mortalité), Tumeurs du sein (métabolisme), Édition de gène (méthodes).
- MESH :
- anatomopathologie : Tumeurs du sein.
- antagonistes et inhibiteurs : Sérine-thréonine kinases TOR.
- génétique : Facteurs d'initiation eucaryotes, Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines, Phosphoprotéines, Protéines adaptatrices de la transduction du signal, Protéines de transport, Sérine-thréonine kinases TOR, Tumeurs du sein.
- mortalité : Tumeurs du sein.
- métabolisme : Facteurs d'initiation eucaryotes, Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines, Phosphoprotéines, Protéines adaptatrices de la transduction du signal, Protéines de transport, Sérine-thréonine kinases TOR, Tumeurs du sein.
- méthodes : Édition de gène.
- pharmacologie : Antibiotiques antinéoplasiques, Indoles, Purines, Sirolimus.
- Analyse de survie, Animaux, Bases de données génétiques, Biosynthèse des protéines, Cellules HeLa, Cellules HepG2, Cellules MCF-7, Femelle, Humains, Mâle, Prolifération cellulaire, Régulation de l'expression des gènes tumoraux, Souris, Souris de lignée C57BL, Systèmes CRISPR-Cas, Transduction du signal.
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (genetics), Adaptor Proteins, Signal Transducing (metabolism), Animals (MeSH), Antibiotics, Antineoplastic (pharmacology), Basic Helix-Loop-Helix Leucine Zipper Transcription Factors (genetics), Basic Helix-Loop-Helix Leucine Zipper Transcription Factors (metabolism), Breast Neoplasms (genetics), Breast Neoplasms (metabolism), Breast Neoplasms (mortality), Breast Neoplasms (pathology), CRISPR-Cas Systems (MeSH), Carrier Proteins (genetics), Carrier Proteins (metabolism), Cell Proliferation (MeSH), Databases, Genetic (MeSH), Eukaryotic Initiation Factors (genetics), Eukaryotic Initiation Factors (metabolism), Female (MeSH), Gene Editing (methods), Gene Expression Regulation, Neoplastic (MeSH), HeLa Cells (MeSH), Hep G2 Cells (MeSH), Humans (MeSH), Indoles (pharmacology), MCF-7 Cells (MeSH), Male (MeSH), Mice (MeSH), Mice, Inbred C57BL (MeSH), Phosphoproteins (genetics), Phosphoproteins (metabolism), Protein Biosynthesis (MeSH), Purines (pharmacology), Signal Transduction (MeSH), Sirolimus (pharmacology), Survival Analysis (MeSH), TOR Serine-Threonine Kinases (antagonists & inhibitors), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (metabolism).
- MESH :
- chemical , antagonists & inhibitors : TOR Serine-Threonine Kinases.
- chemical , genetics : Adaptor Proteins, Signal Transducing, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Carrier Proteins, Eukaryotic Initiation Factors, Phosphoproteins, TOR Serine-Threonine Kinases.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Carrier Proteins, Eukaryotic Initiation Factors, Phosphoproteins, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Antibiotics, Antineoplastic, Indoles, Purines, Sirolimus.
- genetics : Breast Neoplasms.
- metabolism : Breast Neoplasms.
- methods : Gene Editing.
- mortality : Breast Neoplasms.
- pathology : Breast Neoplasms.
- Animals, CRISPR-Cas Systems, Cell Proliferation, Databases, Genetic, Female, Gene Expression Regulation, Neoplastic, HeLa Cells, Hep G2 Cells, Humans, MCF-7 Cells, Male, Mice, Mice, Inbred C57BL, Protein Biosynthesis, Signal Transduction, Survival Analysis.
Abstract
Targeting mTORC1 is a highly promising strategy in cancer therapy. Suppression of mTORC1 activity leads to rapid dephosphorylation of eIF4E-binding proteins (4E-BP1-3) and subsequent inhibition of mRNA translation. However, how the different 4E-BPs affect translation during prolonged use of mTOR inhibitors is not known. Here we show that the expression of 4E-BP3, but not that of 4E-BP1 or 4E-BP2, is transcriptionally induced during prolonged mTORC1 inhibition in vitro and in vivo. Mechanistically, our data reveal that 4E-BP3 expression is controlled by the transcription factor TFE3 through a cis-regulatory element in the EIF4EBP3 gene promoter. CRISPR/Cas9-mediated EIF4EBP3 gene disruption in human cancer cells mitigated the inhibition of translation and proliferation caused by prolonged treatment with mTOR inhibitors. Our findings show that 4E-BP3 is an important effector of mTORC1 and a robust predictive biomarker of therapeutic response to prolonged treatment with mTOR-targeting drugs in cancer.
DOI: 10.1038/ncomms11776
PubMed: 27319316
PubMed Central: PMC4915159
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<term>Adaptor Proteins, Signal Transducing (metabolism)</term>
<term>Animals (MeSH)</term>
<term>Antibiotics, Antineoplastic (pharmacology)</term>
<term>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors (genetics)</term>
<term>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors (metabolism)</term>
<term>Breast Neoplasms (genetics)</term>
<term>Breast Neoplasms (metabolism)</term>
<term>Breast Neoplasms (mortality)</term>
<term>Breast Neoplasms (pathology)</term>
<term>CRISPR-Cas Systems (MeSH)</term>
<term>Carrier Proteins (genetics)</term>
<term>Carrier Proteins (metabolism)</term>
<term>Cell Proliferation (MeSH)</term>
<term>Databases, Genetic (MeSH)</term>
<term>Eukaryotic Initiation Factors (genetics)</term>
<term>Eukaryotic Initiation Factors (metabolism)</term>
<term>Female (MeSH)</term>
<term>Gene Editing (methods)</term>
<term>Gene Expression Regulation, Neoplastic (MeSH)</term>
<term>HeLa Cells (MeSH)</term>
<term>Hep G2 Cells (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Indoles (pharmacology)</term>
<term>MCF-7 Cells (MeSH)</term>
<term>Male (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Phosphoproteins (genetics)</term>
<term>Phosphoproteins (metabolism)</term>
<term>Protein Biosynthesis (MeSH)</term>
<term>Purines (pharmacology)</term>
<term>Signal Transduction (MeSH)</term>
<term>Sirolimus (pharmacology)</term>
<term>Survival Analysis (MeSH)</term>
<term>TOR Serine-Threonine Kinases (antagonists & inhibitors)</term>
<term>TOR Serine-Threonine Kinases (genetics)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Analyse de survie (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Antibiotiques antinéoplasiques (pharmacologie)</term>
<term>Bases de données génétiques (MeSH)</term>
<term>Biosynthèse des protéines (MeSH)</term>
<term>Cellules HeLa (MeSH)</term>
<term>Cellules HepG2 (MeSH)</term>
<term>Cellules MCF-7 (MeSH)</term>
<term>Facteurs d'initiation eucaryotes (génétique)</term>
<term>Facteurs d'initiation eucaryotes (métabolisme)</term>
<term>Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines (génétique)</term>
<term>Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines (métabolisme)</term>
<term>Femelle (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Indoles (pharmacologie)</term>
<term>Mâle (MeSH)</term>
<term>Phosphoprotéines (génétique)</term>
<term>Phosphoprotéines (métabolisme)</term>
<term>Prolifération cellulaire (MeSH)</term>
<term>Protéines adaptatrices de la transduction du signal (génétique)</term>
<term>Protéines adaptatrices de la transduction du signal (métabolisme)</term>
<term>Protéines de transport (génétique)</term>
<term>Protéines de transport (métabolisme)</term>
<term>Purines (pharmacologie)</term>
<term>Régulation de l'expression des gènes tumoraux (MeSH)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Systèmes CRISPR-Cas (MeSH)</term>
<term>Sérine-thréonine kinases TOR (antagonistes et inhibiteurs)</term>
<term>Sérine-thréonine kinases TOR (génétique)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Transduction du signal (MeSH)</term>
<term>Tumeurs du sein (anatomopathologie)</term>
<term>Tumeurs du sein (génétique)</term>
<term>Tumeurs du sein (mortalité)</term>
<term>Tumeurs du sein (métabolisme)</term>
<term>Édition de gène (méthodes)</term>
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</keywords>
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<term>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors</term>
<term>Carrier Proteins</term>
<term>Eukaryotic Initiation Factors</term>
<term>Phosphoproteins</term>
<term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term>
<term>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors</term>
<term>Carrier Proteins</term>
<term>Eukaryotic Initiation Factors</term>
<term>Phosphoproteins</term>
<term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antibiotics, Antineoplastic</term>
<term>Indoles</term>
<term>Purines</term>
<term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs du sein</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Breast Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteurs d'initiation eucaryotes</term>
<term>Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines</term>
<term>Phosphoprotéines</term>
<term>Protéines adaptatrices de la transduction du signal</term>
<term>Protéines de transport</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Tumeurs du sein</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Breast Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Gene Editing</term>
</keywords>
<keywords scheme="MESH" qualifier="mortality" xml:lang="en"><term>Breast Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="mortalité" xml:lang="fr"><term>Tumeurs du sein</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs d'initiation eucaryotes</term>
<term>Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines</term>
<term>Phosphoprotéines</term>
<term>Protéines adaptatrices de la transduction du signal</term>
<term>Protéines de transport</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Tumeurs du sein</term>
</keywords>
<keywords scheme="MESH" qualifier="méthodes" xml:lang="fr"><term>Édition de gène</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Breast Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antibiotiques antinéoplasiques</term>
<term>Indoles</term>
<term>Purines</term>
<term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>CRISPR-Cas Systems</term>
<term>Cell Proliferation</term>
<term>Databases, Genetic</term>
<term>Female</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>HeLa Cells</term>
<term>Hep G2 Cells</term>
<term>Humans</term>
<term>MCF-7 Cells</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Protein Biosynthesis</term>
<term>Signal Transduction</term>
<term>Survival Analysis</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Analyse de survie</term>
<term>Animaux</term>
<term>Bases de données génétiques</term>
<term>Biosynthèse des protéines</term>
<term>Cellules HeLa</term>
<term>Cellules HepG2</term>
<term>Cellules MCF-7</term>
<term>Femelle</term>
<term>Humains</term>
<term>Mâle</term>
<term>Prolifération cellulaire</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Systèmes CRISPR-Cas</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en">Targeting mTORC1 is a highly promising strategy in cancer therapy. Suppression of mTORC1 activity leads to rapid dephosphorylation of eIF4E-binding proteins (4E-BP1-3) and subsequent inhibition of mRNA translation. However, how the different 4E-BPs affect translation during prolonged use of mTOR inhibitors is not known. Here we show that the expression of 4E-BP3, but not that of 4E-BP1 or 4E-BP2, is transcriptionally induced during prolonged mTORC1 inhibition in vitro and in vivo. Mechanistically, our data reveal that 4E-BP3 expression is controlled by the transcription factor TFE3 through a cis-regulatory element in the EIF4EBP3 gene promoter. CRISPR/Cas9-mediated EIF4EBP3 gene disruption in human cancer cells mitigated the inhibition of translation and proliferation caused by prolonged treatment with mTOR inhibitors. Our findings show that 4E-BP3 is an important effector of mTORC1 and a robust predictive biomarker of therapeutic response to prolonged treatment with mTOR-targeting drugs in cancer.</div>
</front>
</TEI>
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<Month>08</Month>
<Day>21</Day>
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<Month>06</Month>
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<Title>Nature communications</Title>
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<ArticleTitle>Translation control during prolonged mTORC1 inhibition mediated by 4E-BP3.</ArticleTitle>
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<ELocationID EIdType="doi" ValidYN="Y">10.1038/ncomms11776</ELocationID>
<Abstract><AbstractText>Targeting mTORC1 is a highly promising strategy in cancer therapy. Suppression of mTORC1 activity leads to rapid dephosphorylation of eIF4E-binding proteins (4E-BP1-3) and subsequent inhibition of mRNA translation. However, how the different 4E-BPs affect translation during prolonged use of mTOR inhibitors is not known. Here we show that the expression of 4E-BP3, but not that of 4E-BP1 or 4E-BP2, is transcriptionally induced during prolonged mTORC1 inhibition in vitro and in vivo. Mechanistically, our data reveal that 4E-BP3 expression is controlled by the transcription factor TFE3 through a cis-regulatory element in the EIF4EBP3 gene promoter. CRISPR/Cas9-mediated EIF4EBP3 gene disruption in human cancer cells mitigated the inhibition of translation and proliferation caused by prolonged treatment with mTOR inhibitors. Our findings show that 4E-BP3 is an important effector of mTORC1 and a robust predictive biomarker of therapeutic response to prolonged treatment with mTOR-targeting drugs in cancer.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tsukumo</LastName>
<ForeName>Yoshinori</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry and Goodman Cancer Research Centre, McGill University, Cancer Pavilion 1160 Pine Avenue West, Montreal, Quebec, Canada H3A 1A3.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Alain</LastName>
<ForeName>Tommy</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, Children's Hospital of Eastern Ontario Research Institute, University of Ottawa, Ottawa, Ontario, Canada K1H 8L1.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fonseca</LastName>
<ForeName>Bruno D</ForeName>
<Initials>BD</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, Children's Hospital of Eastern Ontario Research Institute, University of Ottawa, Ottawa, Ontario, Canada K1H 8L1.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nadon</LastName>
<ForeName>Robert</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>McGill University and Genome Quebec Innovation Centre, Department of Human Genetics, McGill University, Montreal, Quebec, Canada H3A 1A5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sonenberg</LastName>
<ForeName>Nahum</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry and Goodman Cancer Research Centre, McGill University, Cancer Pavilion 1160 Pine Avenue West, Montreal, Quebec, Canada H3A 1A3.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>06</Month>
<Day>20</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Nat Commun</MedlineTA>
<NlmUniqueID>101528555</NlmUniqueID>
<ISSNLinking>2041-1723</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D048868">Adaptor Proteins, Signal Transducing</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000903">Antibiotics, Antineoplastic</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051778">Basic Helix-Loop-Helix Leucine Zipper Transcription Factors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C087000">EIF4EBP1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C104151">EIF4EBP2 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C112661">EIF4EBP3 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D039642">Eukaryotic Initiation Factors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D007211">Indoles</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D011687">Purines</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C069203">TFE3 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="C546842">MTOR protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance>
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<NameOfSubstance UI="C572919">PP242</NameOfSubstance>
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<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000903" MajorTopicYN="N">Antibiotics, Antineoplastic</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051778" MajorTopicYN="N">Basic Helix-Loop-Helix Leucine Zipper Transcription Factors</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001943" MajorTopicYN="N">Breast Neoplasms</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D064113" MajorTopicYN="N">CRISPR-Cas Systems</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002352" MajorTopicYN="N">Carrier Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D030541" MajorTopicYN="N">Databases, Genetic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D039642" MajorTopicYN="N">Eukaryotic Initiation Factors</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000072669" MajorTopicYN="N">Gene Editing</DescriptorName>
<QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015972" MajorTopicYN="Y">Gene Expression Regulation, Neoplastic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006367" MajorTopicYN="N">HeLa Cells</DescriptorName>
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<MeshHeading><DescriptorName UI="D056945" MajorTopicYN="N">Hep G2 Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007211" MajorTopicYN="N">Indoles</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
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<MeshHeading><DescriptorName UI="D061986" MajorTopicYN="N">MCF-7 Cells</DescriptorName>
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<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
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<MeshHeading><DescriptorName UI="D010750" MajorTopicYN="N">Phosphoproteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014176" MajorTopicYN="N">Protein Biosynthesis</DescriptorName>
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<MeshHeading><DescriptorName UI="D011687" MajorTopicYN="N">Purines</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
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<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
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<MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016019" MajorTopicYN="N">Survival Analysis</DescriptorName>
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<MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName>
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<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<PubMedPubDate PubStatus="accepted"><Year>2016</Year>
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<Day>27</Day>
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<name sortKey="Fonseca, Bruno D" sort="Fonseca, Bruno D" uniqKey="Fonseca B" first="Bruno D" last="Fonseca">Bruno D. Fonseca</name>
<name sortKey="Nadon, Robert" sort="Nadon, Robert" uniqKey="Nadon R" first="Robert" last="Nadon">Robert Nadon</name>
<name sortKey="Sonenberg, Nahum" sort="Sonenberg, Nahum" uniqKey="Sonenberg N" first="Nahum" last="Sonenberg">Nahum Sonenberg</name>
</country>
</tree>
</affiliations>
</record>
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