Autophagy in Pancreatic Cancer
Identifieur interne : 000E41 ( Ncbi/Merge ); précédent : 000E40; suivant : 000E42Autophagy in Pancreatic Cancer
Auteurs : Daniel Grasso [France] ; Maria Noé Garcia [France] ; Juan L. Iovanna [France]Source :
- International Journal of Cell Biology [ 1687-8876 ] ; 2012.
Abstract
Pancreatic adenocarcinoma (PDAC) is a devastating disease with an extremely poor life expectancy and no effective treatment. Autophagy is a process of degradation of cytoplasmic component capable of recycling cellular components or eliminate specific targets. The presence of autophagy in PDAC has been demonstrated. However, the implicated cellular pathways are not fully understood and, more importantly, the role of autophagy in PDAC is matter of intensive debate. This review summarizes recently published data in an attempt to clarify the importance of autophagy in this disease and try to reconcile apparently contradictory results.
Url:
DOI: 10.1155/2012/760498
PubMed: 22291707
PubMed Central: 3265076
Links toward previous steps (curation, corpus...)
- to stream Pmc, to step Corpus: 000971
- to stream Pmc, to step Curation: 000967
- to stream Pmc, to step Checkpoint: 000640
Links to Exploration step
PMC:3265076Le document en format XML
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Iovanna</name><affiliation wicri:level="3"><nlm:aff id="I1">Parc Scientifique et Technologique de Luminy, Stress Cellulaire, INSERM U624, 163 avenue de Luminy, CP 915, 13288 Marseille Cedex 9, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea>Parc Scientifique et Technologique de Luminy, Stress Cellulaire, INSERM U624, 163 avenue de Luminy, CP 915, 13288 Marseille Cedex 9</wicri:regionArea><placeName><region type="region" nuts="2">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName></affiliation></author></analytic><series><title level="j">International Journal of Cell Biology</title><idno type="ISSN">1687-8876</idno><idno type="eISSN">1687-8884</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Pancreatic adenocarcinoma (PDAC) is a devastating disease with an extremely poor life expectancy and no effective treatment. Autophagy is a process of degradation of cytoplasmic component capable of recycling cellular components or eliminate specific targets. The presence of autophagy in PDAC has been demonstrated. However, the implicated cellular pathways are not fully understood and, more importantly, the role of autophagy in PDAC is matter of intensive debate. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Int J Cell Biol</journal-id><journal-id journal-id-type="publisher-id">IJCB</journal-id><journal-title-group><journal-title>International Journal of Cell Biology</journal-title></journal-title-group><issn pub-type="ppub">1687-8876</issn><issn pub-type="epub">1687-8884</issn><publisher><publisher-name>Hindawi Publishing Corporation</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">22291707</article-id><article-id pub-id-type="pmc">3265076</article-id><article-id pub-id-type="doi">10.1155/2012/760498</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title>Autophagy in Pancreatic Cancer</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Grasso</surname><given-names>Daniel</given-names></name><xref ref-type="aff" rid="I1"></xref></contrib><contrib contrib-type="author"><name><surname>Garcia</surname><given-names>Maria Noé</given-names></name><xref ref-type="aff" rid="I1"></xref></contrib><contrib contrib-type="author"><name><surname>Iovanna</surname><given-names>Juan L.</given-names></name><xref ref-type="aff" rid="I1"></xref><xref ref-type="corresp" rid="cor1">*</xref></contrib></contrib-group><aff id="I1">Parc Scientifique et Technologique de Luminy, Stress Cellulaire, INSERM U624, 163 avenue de Luminy, CP 915, 13288 Marseille Cedex 9, France</aff><author-notes><corresp id="cor1">*Juan L. Iovanna: <email>juan.iovanna@inserm.fr</email></corresp><fn fn-type="other"><p>Academic Editor: G. S. Stein</p></fn></author-notes><pub-date pub-type="ppub"><year>2012</year></pub-date><pub-date pub-type="epub"><day>16</day><month>1</month><year>2012</year></pub-date><volume>2012</volume><elocation-id>760498</elocation-id><history><date date-type="received"><day>1</day><month>8</month><year>2011</year></date><date date-type="accepted"><day>13</day><month>10</month><year>2011</year></date></history><permissions><copyright-statement>Copyright © 2012 Daniel Grasso et al.</copyright-statement><copyright-year>2012</copyright-year><license license-type="open-access"><license-p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><p>Pancreatic adenocarcinoma (PDAC) is a devastating disease with an extremely poor life expectancy and no effective treatment. Autophagy is a process of degradation of cytoplasmic component capable of recycling cellular components or eliminate specific targets. The presence of autophagy in PDAC has been demonstrated. However, the implicated cellular pathways are not fully understood and, more importantly, the role of autophagy in PDAC is matter of intensive debate. This review summarizes recently published data in an attempt to clarify the importance of autophagy in this disease and try to reconcile apparently contradictory results.</p></abstract></article-meta></front><floats-group><fig id="fig1" position="float"><label>Figure 1</label><caption><p>Hypoxia induces autophagy. Hypoxia activates HIF-1<italic>α</italic> which in turn induces expression of the BH3-containing proteins BNIP3 and BNIP3L to compete with Beclin 1 for its interaction with Bcl2. As a consequence Beclin 1 is released to induce autophagy.</p></caption><graphic xlink:href="IJCB2012-760498.001"></graphic></fig><fig id="fig2" position="float"><label>Figure 2</label><caption><p>HMGB1 and RAGE induce autophagy. HMGB1 is released by necrotic and inflammatory cells. Expression of RAGE is induced by ROS in a NF-kB-dependent manner. On one hand, HMGB1 induces autophagy by its direct binding to the RAGE. On the other hand, HMGB1 induces autophagy by interacting with Beclin 1 which results in dissociation of Beclin 1-Bcl2 and subsequent induction of autophagy.</p></caption><graphic xlink:href="IJCB2012-760498.002"></graphic></fig><fig id="fig3" position="float"><label>Figure 3</label><caption><p>Chemotherapeutics agents induce autophagy. Gemcitabine induces expression of the autophagy starter protein VMP1 and CB1 and CB2 cannabinoids receptors, and production of ROS. Cannabinoids induce autophagy by activating ER stress and enhance gemcitabine action.</p></caption><graphic xlink:href="IJCB2012-760498.003"></graphic></fig><fig id="fig4" position="float"><label>Figure 4</label><caption><p>Autophagy of stromal cells fuel PDAC cells. PDAC release ROS to the tumoral microenvironment to induce autophagy in stromal cells. As consequence, stromal cells provide PDAC cancer cells with a steady stream of recycled nutrients and energy-rich metabolites.</p></caption><graphic xlink:href="IJCB2012-760498.004"></graphic></fig></floats-group></pmc><affiliations><list><country><li>France</li></country><region><li>Provence-Alpes-Côte d'Azur</li></region><settlement><li>Marseille</li></settlement></list><tree><country name="France"><region name="Provence-Alpes-Côte d'Azur"><name sortKey="Grasso, Daniel" sort="Grasso, Daniel" uniqKey="Grasso D" first="Daniel" last="Grasso">Daniel Grasso</name></region><name sortKey="Garcia, Maria Noe" sort="Garcia, Maria Noe" uniqKey="Garcia M" first="Maria Noé" last="Garcia">Maria Noé Garcia</name><name sortKey="Iovanna, Juan L" sort="Iovanna, Juan L" uniqKey="Iovanna J" first="Juan L." last="Iovanna">Juan L. Iovanna</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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