17α-androstenediol-mediated oncophagy of tumor cells by different mechanisms is determined by the target tumor.
Identifieur interne : 001D19 ( Main/Exploration ); précédent : 001D18; suivant : 001D2017α-androstenediol-mediated oncophagy of tumor cells by different mechanisms is determined by the target tumor.
Auteurs : Roger M. Loria [États-Unis] ; Martin R. GrafSource :
- Annals of the New York Academy of Sciences [ 1749-6632 ] ; 2012.
Descripteurs français
- KwdFr :
- Androstènediol (), Androstènediol (pharmacologie), Antinéoplasiques hormonaux (), Antinéoplasiques hormonaux (pharmacologie), Apoptose (), Apoptose (physiologie), Autophagie (), Autophagie (physiologie), Femelle, Humains, Lignée cellulaire tumorale, Prolifération cellulaire (), Relation structure-activité, Stéréoisomérie, Tumeurs (anatomopathologie), Tumeurs (physiopathologie), Tumeurs (traitement médicamenteux).
- MESH :
- anatomopathologie : Tumeurs.
- pharmacologie : Androstènediol, Antinéoplasiques hormonaux.
- physiologie : Apoptose, Autophagie.
- physiopathologie : Tumeurs.
- traitement médicamenteux : Tumeurs.
- Androstènediol, Antinéoplasiques hormonaux, Apoptose, Autophagie, Femelle, Humains, Lignée cellulaire tumorale, Prolifération cellulaire, Relation structure-activité, Stéréoisomérie.
English descriptors
- KwdEn :
- Androstenediol (chemistry), Androstenediol (pharmacology), Antineoplastic Agents, Hormonal (chemistry), Antineoplastic Agents, Hormonal (pharmacology), Apoptosis (drug effects), Apoptosis (physiology), Autophagy (drug effects), Autophagy (physiology), Cell Line, Tumor, Cell Proliferation (drug effects), Female, Humans, Neoplasms (drug therapy), Neoplasms (pathology), Neoplasms (physiopathology), Stereoisomerism, Structure-Activity Relationship.
- MESH :
- chemical , chemistry : Androstenediol, Antineoplastic Agents, Hormonal.
- chemical , pharmacology : Androstenediol, Antineoplastic Agents, Hormonal.
- drug effects : Apoptosis, Autophagy, Cell Proliferation.
- drug therapy : Neoplasms.
- pathology : Neoplasms.
- physiology : Apoptosis, Autophagy.
- physiopathology : Neoplasms.
- Cell Line, Tumor, Female, Humans, Stereoisomerism, Structure-Activity Relationship.
Abstract
Δ5-androstene-3β,17α-diol (17α-AED) mediates oncophagy of human myeloid, glioma, and breast tumor cells by apoptotic- and autophagic-programmed cell death pathways, whereas the 17β-epimer does not. In hematologically derived myeloid tumor cells, 17α-AED induced apoptosis, as determined by TUNEL staining, caspase, PARP activation, and electron microscopy. In contrast, 17α-AED treatment of glioma cells of neuroectodermal lineaged induced autophagy, evident by the presence of acidic vesicular organelles, LC3 processing, and upregulation of beclin-1. Proliferation inhibition studies on primary and established glioma cells demonstrated that the IC-50 of the steroid is ∼15 μM. In the case of breast cancer cells, the bioactivity of 17α-AED is independent of the expression of estrogen or androgen receptors. Collectively, oncophagy is induced by 17α-AED treatment in human tumor cells and proceeds by the induction of either autophagy or apoptosis. The neoplastic cell determines which oncophagic pathway is utilized.
DOI: 10.1111/j.1749-6632.2012.06602.x
PubMed: 22823444
Affiliations:
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Le document en format XML
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Graf</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="doi">10.1111/j.1749-6632.2012.06602.x</idno><idno type="RBID">pubmed:22823444</idno><idno type="pmid">22823444</idno><idno type="wicri:Area/PubMed/Corpus">000086</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000086</idno><idno type="wicri:Area/PubMed/Curation">000086</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000086</idno><idno type="wicri:Area/PubMed/Checkpoint">000089</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000089</idno><idno type="wicri:Area/Ncbi/Merge">000138</idno><idno type="wicri:Area/Ncbi/Curation">000136</idno><idno type="wicri:Area/Ncbi/Checkpoint">000136</idno><idno type="wicri:Area/Main/Merge">001D38</idno><idno type="wicri:Area/Main/Curation">001D19</idno><idno type="wicri:Area/Main/Exploration">001D19</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">17α-androstenediol-mediated oncophagy of tumor cells by different mechanisms is determined by the target tumor.</title><author><name sortKey="Loria, Roger M" sort="Loria, Roger M" uniqKey="Loria R" first="Roger M" last="Loria">Roger M. Loria</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA. loria@vcu.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, Virginia Commonwealth University Medical Center, Richmond, Virginia</wicri:regionArea><placeName><region type="state">Virginie</region></placeName></affiliation></author><author><name sortKey="Graf, Martin R" sort="Graf, Martin R" uniqKey="Graf M" first="Martin R" last="Graf">Martin R. Graf</name></author></analytic><series><title level="j">Annals of the New York Academy of Sciences</title><idno type="eISSN">1749-6632</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Androstenediol (chemistry)</term><term>Androstenediol (pharmacology)</term><term>Antineoplastic Agents, Hormonal (chemistry)</term><term>Antineoplastic Agents, Hormonal (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Apoptosis (physiology)</term><term>Autophagy (drug effects)</term><term>Autophagy (physiology)</term><term>Cell Line, Tumor</term><term>Cell Proliferation (drug effects)</term><term>Female</term><term>Humans</term><term>Neoplasms (drug therapy)</term><term>Neoplasms (pathology)</term><term>Neoplasms (physiopathology)</term><term>Stereoisomerism</term><term>Structure-Activity Relationship</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Androstènediol ()</term><term>Androstènediol (pharmacologie)</term><term>Antinéoplasiques hormonaux ()</term><term>Antinéoplasiques hormonaux (pharmacologie)</term><term>Apoptose ()</term><term>Apoptose (physiologie)</term><term>Autophagie ()</term><term>Autophagie (physiologie)</term><term>Femelle</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Prolifération cellulaire ()</term><term>Relation structure-activité</term><term>Stéréoisomérie</term><term>Tumeurs (anatomopathologie)</term><term>Tumeurs (physiopathologie)</term><term>Tumeurs (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Androstenediol</term><term>Antineoplastic Agents, Hormonal</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Androstenediol</term><term>Antineoplastic Agents, Hormonal</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Proliferation</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Androstènediol</term><term>Antinéoplasiques hormonaux</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Tumeurs</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Female</term><term>Humans</term><term>Stereoisomerism</term><term>Structure-Activity Relationship</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Androstènediol</term><term>Antinéoplasiques hormonaux</term><term>Apoptose</term><term>Autophagie</term><term>Femelle</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Prolifération cellulaire</term><term>Relation structure-activité</term><term>Stéréoisomérie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Δ5-androstene-3β,17α-diol (17α-AED) mediates oncophagy of human myeloid, glioma, and breast tumor cells by apoptotic- and autophagic-programmed cell death pathways, whereas the 17β-epimer does not. In hematologically derived myeloid tumor cells, 17α-AED induced apoptosis, as determined by TUNEL staining, caspase, PARP activation, and electron microscopy. In contrast, 17α-AED treatment of glioma cells of neuroectodermal lineaged induced autophagy, evident by the presence of acidic vesicular organelles, LC3 processing, and upregulation of beclin-1. Proliferation inhibition studies on primary and established glioma cells demonstrated that the IC-50 of the steroid is ∼15 μM. In the case of breast cancer cells, the bioactivity of 17α-AED is independent of the expression of estrogen or androgen receptors. Collectively, oncophagy is induced by 17α-AED treatment in human tumor cells and proceeds by the induction of either autophagy or apoptosis. The neoplastic cell determines which oncophagic pathway is utilized.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Virginie</li></region></list><tree><noCountry><name sortKey="Graf, Martin R" sort="Graf, Martin R" uniqKey="Graf M" first="Martin R" last="Graf">Martin R. Graf</name></noCountry><country name="États-Unis"><region name="Virginie"><name sortKey="Loria, Roger M" sort="Loria, Roger M" uniqKey="Loria R" first="Roger M" last="Loria">Roger M. Loria</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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