Hallmarks of the cancer cell of origin: Comparisons with "energetic" cancer stem cells (e-CSCs).
Identifieur interne : 000159 ( Main/Exploration ); précédent : 000158; suivant : 000160Hallmarks of the cancer cell of origin: Comparisons with "energetic" cancer stem cells (e-CSCs).
Auteurs : Federica Sotgia [Royaume-Uni] ; Marco Fiorillo [Royaume-Uni, Italie] ; Michael P. Lisanti [Royaume-Uni]Source :
- Aging [ 1945-4589 ] ; 2019.
Descripteurs français
- KwdFr :
- MESH :
- physiologie : Cellules souches tumorales.
- étiologie : Tumeurs.
- Humains.
English descriptors
- KwdEn :
- MESH :
- etiology : Neoplasms.
- physiology : Neoplastic Stem Cells.
- Humans.
Abstract
Here, we discuss the expected hallmark(s) of the cancer cell of origin and how this may be related to a new tumor cell phenotype, namely "energetic" cancer stem cells (e-CSCs). e-CSCs show many features that would be characteristic of the cancer cell of origin, including the over-expression of p21-WAF (CDKN1A), a key marker of senescence. It is tempting to speculate that the cancer cell of origin and e-CSCs are closely related entities. e-CSCs possess a hybrid phenotype, sharing key hallmarks of senescence, "stemness" and cancer. e-CSCs are hyper-proliferative and have elevated mitochondrial metabolism, with an NRF2-mediated anti-oxidant response signature, including glutaredoxin (GLRX) and ALDH3A1 over-expression, possibly related to their escape from senescence. Finally, in e-CSCs, BCAS1 (Breast carcinoma-amplified sequence-1) protein expression was up-regulated by >100-fold. BCAS1 is a candidate oncogene associated with "stemness" and aggressive oncogenic behavior, such as Tamoxifen resistance.
DOI: 10.18632/aging.101822
PubMed: 30760648
PubMed Central: PMC6382415
Affiliations:
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Lisanti</name><affiliation wicri:level="4"><nlm:affiliation>Translational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC), University of Salford, Greater Manchester, M5 4WT, United Kingdom.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Translational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC), University of Salford, Greater Manchester, M5 4WT</wicri:regionArea><orgName type="university">Université de Salford</orgName><placeName><settlement type="city">Manchester</settlement><settlement type="town">Salford</settlement><region type="nation">Angleterre</region><region nuts="2" type="region">Grand Manchester</region></placeName></affiliation></author></analytic><series><title level="j">Aging</title><idno type="eISSN">1945-4589</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Humans (MeSH)</term><term>Neoplasms (etiology)</term><term>Neoplastic Stem Cells (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Cellules souches tumorales (physiologie)</term><term>Humains (MeSH)</term><term>Tumeurs (étiologie)</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Cellules souches tumorales</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Neoplastic Stem Cells</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Tumeurs</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Here, we discuss the expected hallmark(s) of the cancer cell of origin and how this may be related to a new tumor cell phenotype, namely "energetic" cancer stem cells (e-CSCs). e-CSCs show many features that would be characteristic of the cancer cell of origin, including the over-expression of p21-WAF (CDKN1A), a key marker of senescence. It is tempting to speculate that the cancer cell of origin and e-CSCs are closely related entities. e-CSCs possess a hybrid phenotype, sharing key hallmarks of senescence, "stemness" and cancer. e-CSCs are hyper-proliferative and have elevated mitochondrial metabolism, with an NRF2-mediated anti-oxidant response signature, including glutaredoxin (GLRX) and ALDH3A1 over-expression, possibly related to their escape from senescence. Finally, in e-CSCs, BCAS1 (Breast carcinoma-amplified sequence-1) protein expression was up-regulated by >100-fold. BCAS1 is a candidate oncogene associated with "stemness" and aggressive oncogenic behavior, such as Tamoxifen resistance.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30760648</PMID><DateCompleted><Year>2020</Year><Month>04</Month><Day>15</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1945-4589</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><Issue>3</Issue><PubDate><Year>2019</Year><Month>02</Month><Day>13</Day></PubDate></JournalIssue><Title>Aging</Title><ISOAbbreviation>Aging (Albany NY)</ISOAbbreviation></Journal><ArticleTitle>Hallmarks of the cancer cell of origin: Comparisons with "energetic" cancer stem cells (e-CSCs).</ArticleTitle><Pagination><MedlinePgn>1065-1068</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.18632/aging.101822</ELocationID><Abstract><AbstractText>Here, we discuss the expected hallmark(s) of the cancer cell of origin and how this may be related to a new tumor cell phenotype, namely "energetic" cancer stem cells (e-CSCs). e-CSCs show many features that would be characteristic of the cancer cell of origin, including the over-expression of p21-WAF (CDKN1A), a key marker of senescence. It is tempting to speculate that the cancer cell of origin and e-CSCs are closely related entities. e-CSCs possess a hybrid phenotype, sharing key hallmarks of senescence, "stemness" and cancer. e-CSCs are hyper-proliferative and have elevated mitochondrial metabolism, with an NRF2-mediated anti-oxidant response signature, including glutaredoxin (GLRX) and ALDH3A1 over-expression, possibly related to their escape from senescence. Finally, in e-CSCs, BCAS1 (Breast carcinoma-amplified sequence-1) protein expression was up-regulated by >100-fold. BCAS1 is a candidate oncogene associated with "stemness" and aggressive oncogenic behavior, such as Tamoxifen resistance.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sotgia</LastName><ForeName>Federica</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Translational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC), University of Salford, Greater Manchester, M5 4WT, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fiorillo</LastName><ForeName>Marco</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Translational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC), University of Salford, Greater Manchester, M5 4WT, United Kingdom.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Department of Pharmacy, Health and Nutritional Sciences, The University of Calabria, Cosenza, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lisanti</LastName><ForeName>Michael P</ForeName><Initials>MP</Initials><AffiliationInfo><Affiliation>Translational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC), University of Salford, Greater Manchester, M5 4WT, United Kingdom.</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></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Aging (Albany NY)</MedlineTA><NlmUniqueID>101508617</NlmUniqueID><ISSNLinking>1945-4589</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009369" MajorTopicYN="N">Neoplasms</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014411" MajorTopicYN="N">Neoplastic Stem Cells</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">anti-oxidant response</Keyword><Keyword MajorTopicYN="Y">cancer cell of origin</Keyword><Keyword MajorTopicYN="Y">cancer stem cells (CSCs)</Keyword><Keyword MajorTopicYN="Y">metabolism</Keyword><Keyword MajorTopicYN="Y">senescence</Keyword><Keyword MajorTopicYN="Y">tamoxifen resistance</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>01</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>02</Month><Day>07</Day></PubMedPubDate><PubMedPubDate 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Lisanti</name></country><country name="Italie"><noRegion><name sortKey="Fiorillo, Marco" sort="Fiorillo, Marco" uniqKey="Fiorillo M" first="Marco" last="Fiorillo">Marco Fiorillo</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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