Modulation of pediatric brain tumor autophagy and chemosensitivity
Identifieur interne : 001537 ( Main/Exploration ); précédent : 001536; suivant : 001538Modulation of pediatric brain tumor autophagy and chemosensitivity
Auteurs : Jean M. Mulcahy Levy [États-Unis] ; Andrew Thorburn [États-Unis]Source :
- Journal of Neuro-Oncology [ 0167-594X ] ; 2012-01-01.
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Abstract
Abstract: Brain and spinal tumors are the second most common malignancies in childhood after leukemia, and they remain the leading cause of death from childhood cancer. Autophagy is a catabolic cellular process that is thought to regulate chemosensitivity, however its role in pediatric tumors is unknown. Here we present studies in pediatric medulloblastoma cell lines (DAOY, ONS76) and atypical teratoid/rhabdoid tumor cell lines (BT-16, BT-12) to test this role. Autophagy was inhibited using siRNA against autophagy-related genes ATG12 and ATG7 or pharmacologically induced or inhibited using rapamycin and chloroquine to test the effect of autophagy on chemosensitivity. Autophagic flux was measured using Western blot analysis of LC3-II and p62 and cell viability was determined using MTS assays and clonogenic growth. We found that when pediatric brain tumor cells under starvation stress, exposed to known autophagy inducers such as rapamycin, or treated with current chemotherapeutics (lomustine, cisplatin), all stimulate autophagy. Silencing ATG12 and ATG7 or exposure to a known autophagy inhibitor, chloroquine, could inhibit this autophagy increase; however, the effect of autophagy on tumor cell killing was small. These results may have clinical relevance in the future planning of therapeutic regimens for pediatric brain tumors.
Url:
DOI: 10.1007/s11060-011-0684-4
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Mulcahy Levy</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pediatrics, University of Colorado, 12801 E 17th Ave, RC-1 South, Rm 6400D, Mail Stop 8303, 80045, Aurora, CO</wicri:regionArea><placeName><region type="state">Colorado</region></placeName></affiliation></author><author><name sortKey="Thorburn, Andrew" sort="Thorburn, Andrew" uniqKey="Thorburn A" first="Andrew" last="Thorburn">Andrew Thorburn</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pharmacology, University of Colorado, 12801 E 17th Ave, RC-1 South, Rm 6400D, Mail Stop 8303, 80045, Aurora, CO</wicri:regionArea><placeName><region type="state">Colorado</region></placeName></affiliation><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neuro-Oncology</title><title level="j" type="abbrev">J Neurooncol</title><idno type="ISSN">0167-594X</idno><idno type="eISSN">1573-7373</idno><imprint><publisher>Springer US; http://www.springer-ny.com</publisher><pubPlace>Boston</pubPlace><date type="published" when="2012-01-01">2012-01-01</date><biblScope unit="volume">106</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="281">281</biblScope><biblScope unit="page" to="290">290</biblScope></imprint><idno type="ISSN">0167-594X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0167-594X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Atypical teratoid/rhabdoid tumor</term><term>Autophagy</term><term>Brain tumor</term><term>Chemosensitivity</term><term>Medulloblastoma</term><term>Pediatric</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Brain and spinal tumors are the second most common malignancies in childhood after leukemia, and they remain the leading cause of death from childhood cancer. Autophagy is a catabolic cellular process that is thought to regulate chemosensitivity, however its role in pediatric tumors is unknown. Here we present studies in pediatric medulloblastoma cell lines (DAOY, ONS76) and atypical teratoid/rhabdoid tumor cell lines (BT-16, BT-12) to test this role. Autophagy was inhibited using siRNA against autophagy-related genes ATG12 and ATG7 or pharmacologically induced or inhibited using rapamycin and chloroquine to test the effect of autophagy on chemosensitivity. Autophagic flux was measured using Western blot analysis of LC3-II and p62 and cell viability was determined using MTS assays and clonogenic growth. We found that when pediatric brain tumor cells under starvation stress, exposed to known autophagy inducers such as rapamycin, or treated with current chemotherapeutics (lomustine, cisplatin), all stimulate autophagy. Silencing ATG12 and ATG7 or exposure to a known autophagy inhibitor, chloroquine, could inhibit this autophagy increase; however, the effect of autophagy on tumor cell killing was small. These results may have clinical relevance in the future planning of therapeutic regimens for pediatric brain tumors.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Colorado</li></region></list><tree><country name="États-Unis"><region name="Colorado"><name sortKey="Levy, Jean M Mulcahy" sort="Levy, Jean M Mulcahy" uniqKey="Levy J" first="Jean M. Mulcahy" last="Levy">Jean M. Mulcahy Levy</name></region><name sortKey="Thorburn, Andrew" sort="Thorburn, Andrew" uniqKey="Thorburn A" first="Andrew" last="Thorburn">Andrew Thorburn</name><name sortKey="Thorburn, Andrew" sort="Thorburn, Andrew" uniqKey="Thorburn A" first="Andrew" last="Thorburn">Andrew Thorburn</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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