RapamycinFungusV1, Main, Exploration, bibRecord, 000337

HDAC6 differentially regulates autophagy in stem-like versus differentiated cancer cells.

Identifieur interne : 000337 ( Main/Exploration ); précédent : 000336; suivant : 000338

HDAC6 differentially regulates autophagy in stem-like versus differentiated cancer cells.

Auteurs : Tanveer Sharif [Canada] ; Emma Martell [Canada] ; Cathleen Dai [Canada] ; Mohammad Saleh Ghassemi-Rad [Canada] ; Mark Robert Hanes [Canada] ; Patrick J. Murphy [Canada] ; Nandini N. Margam [Canada] ; Hirendrasinh B. Parmar [Canada] ; Carman A. Giacomantonio [Canada] ; Roy Duncan [Canada] ; Patrick W K. Lee [Canada] ; Shashi Gujar [Canada]

Source :

Autophagy [ 1554-8635 ] ; 2019.

RBID : pubmed:30444165

Descripteurs français

English descriptors

Abstract

Cancer stem-like cells (CSCs), a small population of pluripotent cells residing within heterogeneous tumor mass, remain highly resistant to various chemotherapies as compared to the differentiated cancer cells. It is being postulated that CSCs possess unique molecular mechanisms, such as autophagic homeostasis, that allow CSCs to withstand the therapeutic assaults. Here we demonstrate that HDAC6 inhibition differentially modulates macroautophagy/autophagy in CSCs as compared to that of differentiated cancer cells. Using human and murine CSC models and differentiated cells, we show that the inhibition or knockdown (KD) of HDAC6 decreases CSC pluripotency by downregulating major pluripotency factors POU5F1, NANOG and SOX2. This decreased HDAC6 expression increases ACTB, TUBB3 and CSN2 expression and promotes differentiation in CSCs in an apoptosis-independent manner. Mechanistically, HDAC6 KD in CSCs decreases pluripotency by promoting autophagy, whereas the inhibition of pluripotency via retinoic acid treatment, POU5F1 or autophagy-related gene (ATG7 and ATG12) KD in CSCs decreases HDAC6 expression and promotes differentiation. Interestingly, HDAC6 KD-mediated CSC growth inhibition is further enhanced in the presence of autophagy inducers Tat-Beclin 1 peptide and rapamycin. In contrast to the results observed in CSCs, HDAC6 KD in differentiated breast cancer cells downregulates autophagy and increases apoptosis. Furthermore, the autophagy regulator p-MTOR, upstream negative regulators of p-MTOR (TSC1 and TSC2) and downstream effectors of p-MTOR (p-RPS6KB and p-EIF4EBP1) are differentially regulated in CSCs versus differentiated cancer cells following HDAC6 KD. Overall these data identify the differential regulation of autophagy as a molecular link behind the differing chemo-susceptibility of CSCs and differentiated cancer cells.

DOI: 10.1080/15548627.2018.1548547
PubMed: 30444165
PubMed Central: PMC6526821

Affiliations:

Canada

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

to stream Main, to step Corpus: 000405
to stream Main, to step Curation: 000405

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en">HDAC6 differentially regulates autophagy in stem-like versus differentiated cancer cells.</title>
<author><name sortKey="Sharif, Tanveer" sort="Sharif, Tanveer" uniqKey="Sharif T" first="Tanveer" last="Sharif">Tanveer Sharif</name>
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<wicri:noRegion>Nova Scotia </wicri:noRegion>
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<author><name sortKey="Martell, Emma" sort="Martell, Emma" uniqKey="Martell E" first="Emma" last="Martell">Emma Martell</name>
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<country xml:lang="fr">Canada</country>
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<wicri:noRegion>Nova Scotia </wicri:noRegion>
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<author><name sortKey="Dai, Cathleen" sort="Dai, Cathleen" uniqKey="Dai C" first="Cathleen" last="Dai">Cathleen Dai</name>
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<country xml:lang="fr">Canada</country>
<wicri:regionArea>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia </wicri:regionArea>
<wicri:noRegion>Nova Scotia </wicri:noRegion>
</affiliation>
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<author><name sortKey="Ghassemi Rad, Mohammad Saleh" sort="Ghassemi Rad, Mohammad Saleh" uniqKey="Ghassemi Rad M" first="Mohammad Saleh" last="Ghassemi-Rad">Mohammad Saleh Ghassemi-Rad</name>
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<country xml:lang="fr">Canada</country>
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</affiliation>
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<author><name sortKey="Hanes, Mark Robert" sort="Hanes, Mark Robert" uniqKey="Hanes M" first="Mark Robert" last="Hanes">Mark Robert Hanes</name>
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<wicri:noRegion>Nova Scotia </wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Murphy, Patrick J" sort="Murphy, Patrick J" uniqKey="Murphy P" first="Patrick J" last="Murphy">Patrick J. Murphy</name>
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<country xml:lang="fr">Canada</country>
<wicri:regionArea>a Deaprtment of Pathology , Dalhousie University , Halifax , Nova Scotia </wicri:regionArea>
<wicri:noRegion>Nova Scotia </wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Margam, Nandini N" sort="Margam, Nandini N" uniqKey="Margam N" first="Nandini N" last="Margam">Nandini N. Margam</name>
<affiliation wicri:level="1"><nlm:affiliation>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia </wicri:regionArea>
<wicri:noRegion>Nova Scotia </wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Parmar, Hirendrasinh B" sort="Parmar, Hirendrasinh B" uniqKey="Parmar H" first="Hirendrasinh B" last="Parmar">Hirendrasinh B. Parmar</name>
<affiliation wicri:level="1"><nlm:affiliation>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia </wicri:regionArea>
<wicri:noRegion>Nova Scotia </wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Giacomantonio, Carman A" sort="Giacomantonio, Carman A" uniqKey="Giacomantonio C" first="Carman A" last="Giacomantonio">Carman A. Giacomantonio</name>
<affiliation wicri:level="1"><nlm:affiliation>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia </wicri:regionArea>
<wicri:noRegion>Nova Scotia </wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>c Surgery , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation>
<country xml:lang="fr">Canada</country>
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<wicri:noRegion>Nova Scotia </wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Duncan, Roy" sort="Duncan, Roy" uniqKey="Duncan R" first="Roy" last="Duncan">Roy Duncan</name>
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<country xml:lang="fr">Canada</country>
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</affiliation>
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<country xml:lang="fr">Canada</country>
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</affiliation>
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<country xml:lang="fr">Canada</country>
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<wicri:noRegion>Nova Scotia </wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Lee, Patrick W K" sort="Lee, Patrick W K" uniqKey="Lee P" first="Patrick W K" last="Lee">Patrick W K. Lee</name>
<affiliation wicri:level="1"><nlm:affiliation>a Deaprtment of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>a Deaprtment of Pathology , Dalhousie University , Halifax , Nova Scotia </wicri:regionArea>
<wicri:noRegion>Nova Scotia </wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia </wicri:regionArea>
<wicri:noRegion>Nova Scotia </wicri:noRegion>
</affiliation>
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<author><name sortKey="Gujar, Shashi" sort="Gujar, Shashi" uniqKey="Gujar S" first="Shashi" last="Gujar">Shashi Gujar</name>
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<country xml:lang="fr">Canada</country>
<wicri:regionArea>a Deaprtment of Pathology , Dalhousie University , Halifax , Nova Scotia </wicri:regionArea>
<wicri:noRegion>Nova Scotia </wicri:noRegion>
</affiliation>
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<country xml:lang="fr">Canada</country>
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</affiliation>
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<wicri:noRegion>Nova Scotia </wicri:noRegion>
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</analytic>
<series><title level="j">Autophagy</title>
<idno type="eISSN">1554-8635</idno>
<imprint><date when="2019" type="published">2019</date>
</imprint>
</series>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Actins (metabolism)</term>
<term>Animals (MeSH)</term>
<term>Apoptosis (genetics)</term>
<term>Autophagy (genetics)</term>
<term>Autophagy-Related Protein 12 (genetics)</term>
<term>Autophagy-Related Protein 12 (metabolism)</term>
<term>Autophagy-Related Protein 7 (genetics)</term>
<term>Autophagy-Related Protein 7 (metabolism)</term>
<term>Breast Neoplasms (genetics)</term>
<term>Breast Neoplasms (metabolism)</term>
<term>Cell Differentiation (genetics)</term>
<term>Cell Survival (genetics)</term>
<term>Female (MeSH)</term>
<term>HEK293 Cells (MeSH)</term>
<term>Histone Deacetylase 6 (antagonists & inhibitors)</term>
<term>Histone Deacetylase 6 (genetics)</term>
<term>Histone Deacetylase 6 (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Nanog Homeobox Protein (genetics)</term>
<term>Nanog Homeobox Protein (metabolism)</term>
<term>Neoplastic Stem Cells (metabolism)</term>
<term>Octamer Transcription Factor-3 (genetics)</term>
<term>Octamer Transcription Factor-3 (metabolism)</term>
<term>Proteome (metabolism)</term>
<term>SOXB1 Transcription Factors (genetics)</term>
<term>SOXB1 Transcription Factors (metabolism)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Tuberous Sclerosis Complex 1 Protein (antagonists & inhibitors)</term>
<term>Tuberous Sclerosis Complex 1 Protein (genetics)</term>
<term>Tuberous Sclerosis Complex 1 Protein (metabolism)</term>
<term>Tuberous Sclerosis Complex 2 Protein (antagonists & inhibitors)</term>
<term>Tuberous Sclerosis Complex 2 Protein (genetics)</term>
<term>Tuberous Sclerosis Complex 2 Protein (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Actines (métabolisme)</term>
<term>Animaux (MeSH)</term>
<term>Apoptose (génétique)</term>
<term>Autophagie (génétique)</term>
<term>Cellules HEK293 (MeSH)</term>
<term>Cellules souches tumorales (métabolisme)</term>
<term>Différenciation cellulaire (génétique)</term>
<term>Facteur de transcription Oct-3 (génétique)</term>
<term>Facteur de transcription Oct-3 (métabolisme)</term>
<term>Facteurs de transcription SOX-B1 (génétique)</term>
<term>Facteurs de transcription SOX-B1 (métabolisme)</term>
<term>Femelle (MeSH)</term>
<term>Histone deacetylase 6 (antagonistes et inhibiteurs)</term>
<term>Histone deacetylase 6 (génétique)</term>
<term>Histone deacetylase 6 (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Protéine homéotique Nanog (génétique)</term>
<term>Protéine homéotique Nanog (métabolisme)</term>
<term>Protéine-1 du complexe de la sclérose tubéreuse (antagonistes et inhibiteurs)</term>
<term>Protéine-1 du complexe de la sclérose tubéreuse (génétique)</term>
<term>Protéine-1 du complexe de la sclérose tubéreuse (métabolisme)</term>
<term>Protéine-12 associée à l'autophagie (génétique)</term>
<term>Protéine-12 associée à l'autophagie (métabolisme)</term>
<term>Protéine-2 du complexe de la sclérose tubéreuse (antagonistes et inhibiteurs)</term>
<term>Protéine-2 du complexe de la sclérose tubéreuse (génétique)</term>
<term>Protéine-2 du complexe de la sclérose tubéreuse (métabolisme)</term>
<term>Protéine-7 associée à l'autophagie (génétique)</term>
<term>Protéine-7 associée à l'autophagie (métabolisme)</term>
<term>Protéome (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Survie cellulaire (génétique)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Tumeurs du sein (génétique)</term>
<term>Tumeurs du sein (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Histone Deacetylase 6</term>
<term>Tuberous Sclerosis Complex 1 Protein</term>
<term>Tuberous Sclerosis Complex 2 Protein</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Autophagy-Related Protein 12</term>
<term>Autophagy-Related Protein 7</term>
<term>Histone Deacetylase 6</term>
<term>Nanog Homeobox Protein</term>
<term>Octamer Transcription Factor-3</term>
<term>SOXB1 Transcription Factors</term>
<term>Tuberous Sclerosis Complex 1 Protein</term>
<term>Tuberous Sclerosis Complex 2 Protein</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Actins</term>
<term>Autophagy-Related Protein 12</term>
<term>Autophagy-Related Protein 7</term>
<term>Histone Deacetylase 6</term>
<term>Nanog Homeobox Protein</term>
<term>Octamer Transcription Factor-3</term>
<term>Proteome</term>
<term>SOXB1 Transcription Factors</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Tuberous Sclerosis Complex 1 Protein</term>
<term>Tuberous Sclerosis Complex 2 Protein</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Histone deacetylase 6</term>
<term>Protéine-1 du complexe de la sclérose tubéreuse</term>
<term>Protéine-2 du complexe de la sclérose tubéreuse</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Apoptosis</term>
<term>Autophagy</term>
<term>Breast Neoplasms</term>
<term>Cell Differentiation</term>
<term>Cell Survival</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Apoptose</term>
<term>Autophagie</term>
<term>Différenciation cellulaire</term>
<term>Facteur de transcription Oct-3</term>
<term>Facteurs de transcription SOX-B1</term>
<term>Histone deacetylase 6</term>
<term>Protéine homéotique Nanog</term>
<term>Protéine-1 du complexe de la sclérose tubéreuse</term>
<term>Protéine-12 associée à l'autophagie</term>
<term>Protéine-2 du complexe de la sclérose tubéreuse</term>
<term>Protéine-7 associée à l'autophagie</term>
<term>Survie cellulaire</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>Actines</term>
<term>Cellules souches tumorales</term>
<term>Facteur de transcription Oct-3</term>
<term>Facteurs de transcription SOX-B1</term>
<term>Histone deacetylase 6</term>
<term>Protéine homéotique Nanog</term>
<term>Protéine-1 du complexe de la sclérose tubéreuse</term>
<term>Protéine-12 associée à l'autophagie</term>
<term>Protéine-2 du complexe de la sclérose tubéreuse</term>
<term>Protéine-7 associée à l'autophagie</term>
<term>Protéome</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Tumeurs du sein</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Female</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>Mice</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules HEK293</term>
<term>Femelle</term>
<term>Humains</term>
<term>Souris</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Cancer stem-like cells (CSCs), a small population of pluripotent cells residing within heterogeneous tumor mass, remain highly resistant to various chemotherapies as compared to the differentiated cancer cells. It is being postulated that CSCs possess unique molecular mechanisms, such as autophagic homeostasis, that allow CSCs to withstand the therapeutic assaults. Here we demonstrate that HDAC6 inhibition differentially modulates macroautophagy/autophagy in CSCs as compared to that of differentiated cancer cells. Using human and murine CSC models and differentiated cells, we show that the inhibition or knockdown (KD) of HDAC6 decreases CSC pluripotency by downregulating major pluripotency factors POU5F1, NANOG and SOX2. This decreased HDAC6 expression increases ACTB, TUBB3 and CSN2 expression and promotes differentiation in CSCs in an apoptosis-independent manner. Mechanistically, HDAC6 KD in CSCs decreases pluripotency by promoting autophagy, whereas the inhibition of pluripotency via retinoic acid treatment, POU5F1 or autophagy-related gene (ATG7 and ATG12) KD in CSCs decreases HDAC6 expression and promotes differentiation. Interestingly, HDAC6 KD-mediated CSC growth inhibition is further enhanced in the presence of autophagy inducers Tat-Beclin 1 peptide and rapamycin. In contrast to the results observed in CSCs, HDAC6 KD in differentiated breast cancer cells downregulates autophagy and increases apoptosis. Furthermore, the autophagy regulator p-MTOR, upstream negative regulators of p-MTOR (TSC1 and TSC2) and downstream effectors of p-MTOR (p-RPS6KB and p-EIF4EBP1) are differentially regulated in CSCs versus differentiated cancer cells following HDAC6 KD. Overall these data identify the differential regulation of autophagy as a molecular link behind the differing chemo-susceptibility of CSCs and differentiated cancer cells.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30444165</PMID>
<DateCompleted><Year>2020</Year>
<Month>05</Month>
<Day>11</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>05</Month>
<Day>11</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1554-8635</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>15</Volume>
<Issue>4</Issue>
<PubDate><Year>2019</Year>
<Month>04</Month>
</PubDate>
</JournalIssue>
<Title>Autophagy</Title>
<ISOAbbreviation>Autophagy</ISOAbbreviation>
</Journal>
<ArticleTitle>HDAC6 differentially regulates autophagy in stem-like versus differentiated cancer cells.</ArticleTitle>
<Pagination><MedlinePgn>686-706</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1080/15548627.2018.1548547</ELocationID>
<Abstract><AbstractText>Cancer stem-like cells (CSCs), a small population of pluripotent cells residing within heterogeneous tumor mass, remain highly resistant to various chemotherapies as compared to the differentiated cancer cells. It is being postulated that CSCs possess unique molecular mechanisms, such as autophagic homeostasis, that allow CSCs to withstand the therapeutic assaults. Here we demonstrate that HDAC6 inhibition differentially modulates macroautophagy/autophagy in CSCs as compared to that of differentiated cancer cells. Using human and murine CSC models and differentiated cells, we show that the inhibition or knockdown (KD) of HDAC6 decreases CSC pluripotency by downregulating major pluripotency factors POU5F1, NANOG and SOX2. This decreased HDAC6 expression increases ACTB, TUBB3 and CSN2 expression and promotes differentiation in CSCs in an apoptosis-independent manner. Mechanistically, HDAC6 KD in CSCs decreases pluripotency by promoting autophagy, whereas the inhibition of pluripotency via retinoic acid treatment, POU5F1 or autophagy-related gene (ATG7 and ATG12) KD in CSCs decreases HDAC6 expression and promotes differentiation. Interestingly, HDAC6 KD-mediated CSC growth inhibition is further enhanced in the presence of autophagy inducers Tat-Beclin 1 peptide and rapamycin. In contrast to the results observed in CSCs, HDAC6 KD in differentiated breast cancer cells downregulates autophagy and increases apoptosis. Furthermore, the autophagy regulator p-MTOR, upstream negative regulators of p-MTOR (TSC1 and TSC2) and downstream effectors of p-MTOR (p-RPS6KB and p-EIF4EBP1) are differentially regulated in CSCs versus differentiated cancer cells following HDAC6 KD. Overall these data identify the differential regulation of autophagy as a molecular link behind the differing chemo-susceptibility of CSCs and differentiated cancer cells.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sharif</LastName>
<ForeName>Tanveer</ForeName>
<Initials>T</Initials>
<Identifier Source="ORCID">0000-0002-0981-5615</Identifier>
<AffiliationInfo><Affiliation>a Deaprtment of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Martell</LastName>
<ForeName>Emma</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>a Deaprtment of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dai</LastName>
<ForeName>Cathleen</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ghassemi-Rad</LastName>
<ForeName>Mohammad Saleh</ForeName>
<Initials>MS</Initials>
<AffiliationInfo><Affiliation>a Deaprtment of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hanes</LastName>
<ForeName>Mark Robert</ForeName>
<Initials>MR</Initials>
<AffiliationInfo><Affiliation>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Murphy</LastName>
<ForeName>Patrick J</ForeName>
<Initials>PJ</Initials>
<AffiliationInfo><Affiliation>a Deaprtment of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Margam</LastName>
<ForeName>Nandini N</ForeName>
<Initials>NN</Initials>
<AffiliationInfo><Affiliation>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Parmar</LastName>
<ForeName>Hirendrasinh B</ForeName>
<Initials>HB</Initials>
<AffiliationInfo><Affiliation>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Giacomantonio</LastName>
<ForeName>Carman A</ForeName>
<Initials>CA</Initials>
<AffiliationInfo><Affiliation>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>c Surgery , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Duncan</LastName>
<ForeName>Roy</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>d Biochemistry and Molecular Biology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>e Pediatrics , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lee</LastName>
<ForeName>Patrick W K</ForeName>
<Initials>PWK</Initials>
<AffiliationInfo><Affiliation>a Deaprtment of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gujar</LastName>
<ForeName>Shashi</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>a Deaprtment of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>b Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>f Biology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>g Centre for Innovative and Collaborative Health Systems Research , IWK Health Centre , Halifax , Nova Scotia , Canada.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><Acronym>CAPMC</Acronym>
<Agency> CIHR</Agency>
<Country>Canada</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>12</Month>
<Day>04</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Autophagy</MedlineTA>
<NlmUniqueID>101265188</NlmUniqueID>
<ISSNLinking>1554-8627</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C466624">ATG12 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000199">Actins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071192">Autophagy-Related Protein 12</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071317">Nanog Homeobox Protein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D050814">Octamer Transcription Factor-3</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D020543">Proteome</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D055748">SOXB1 Transcription Factors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C000624650">TSC1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C000624653">TSC2 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000077004">Tuberous Sclerosis Complex 1 Protein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000077005">Tuberous Sclerosis Complex 2 Protein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.5.1.98</RegistryNumber>
<NameOfSubstance UI="C433811">HDAC6 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.5.1.98</RegistryNumber>
<NameOfSubstance UI="C499033">Hdac6 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.5.1.98</RegistryNumber>
<NameOfSubstance UI="D000073864">Histone Deacetylase 6</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 6.2.1.45</RegistryNumber>
<NameOfSubstance UI="C509349">Atg7 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 6.2.1.45</RegistryNumber>
<NameOfSubstance UI="D000071193">Autophagy-Related Protein 7</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000199" MajorTopicYN="N">Actins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071192" MajorTopicYN="N">Autophagy-Related Protein 12</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071193" MajorTopicYN="N">Autophagy-Related Protein 7</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001943" MajorTopicYN="N">Breast Neoplasms</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D057809" MajorTopicYN="N">HEK293 Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000073864" MajorTopicYN="N">Histone Deacetylase 6</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071317" MajorTopicYN="N">Nanog Homeobox Protein</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014411" MajorTopicYN="N">Neoplastic Stem Cells</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D050814" MajorTopicYN="N">Octamer Transcription Factor-3</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020543" MajorTopicYN="N">Proteome</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D055748" MajorTopicYN="N">SOXB1 Transcription Factors</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000077004" MajorTopicYN="N">Tuberous Sclerosis Complex 1 Protein</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000077005" MajorTopicYN="N">Tuberous Sclerosis Complex 2 Protein</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Autophagy</Keyword>
<Keyword MajorTopicYN="Y">HDAC6</Keyword>
<Keyword MajorTopicYN="Y">cancer stem-like cells</Keyword>
<Keyword MajorTopicYN="Y">differentiation</Keyword>
<Keyword MajorTopicYN="Y">p-MTOR</Keyword>
<Keyword MajorTopicYN="Y">pluripotency</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2018</Year>
<Month>11</Month>
<Day>18</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2020</Year>
<Month>5</Month>
<Day>12</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2018</Year>
<Month>11</Month>
<Day>17</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
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<ArticleId IdType="doi">10.1080/15548627.2018.1548547</ArticleId>
<ArticleId IdType="pmc">PMC6526821</ArticleId>
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HDAC6 differentially regulates autophagy in stem-like versus differentiated cancer cells.

HDAC6 differentially regulates autophagy in stem-like versus differentiated cancer cells.

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