Inhibition of 6-phosphofructo-2-kinase (PFKFB3) induces autophagy as a survival mechanism.
Identifieur interne : 001020 ( Main/Exploration ); précédent : 001019; suivant : 001021Inhibition of 6-phosphofructo-2-kinase (PFKFB3) induces autophagy as a survival mechanism.
Auteurs : Alden C. Klarer ; Julie O'Neal ; Yoannis Imbert-Fernandez ; Amy Clem ; Steve R. Ellis ; Jennifer Clark ; Brian Clem ; Jason Chesney [États-Unis] ; Sucheta TelangSource :
- Cancer & metabolism [ 2049-3002 ] ; 2014.
Abstract
Unlike glycolytic enzymes that directly catabolize glucose to pyruvate, the family of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases (PFKFBs) control the conversion of fructose-6-phosphate to and from fructose-2,6-bisphosphate, a key regulator of the glycolytic enzyme phosphofructokinase-1 (PFK-1). One family member, PFKFB3, has been shown to be highly expressed and activated in human cancer cells, and derivatives of a PFKFB3 inhibitor, 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO), are currently being developed in clinical trials. However, the effectiveness of drugs such as 3PO that target energetic pathways is limited by survival pathways that can be activated by reduced ATP and nutrient uptake. One such pathway is the process of cellular self-catabolism termed autophagy. We hypothesized that the functional glucose starvation induced by inhibition of PFKFB3 in tumor cells would induce autophagy as a pro-survival mechanism and that inhibitors of autophagy could increase the anti-tumor effects of PFKFB3 inhibitors.
DOI: 10.1186/2049-3002-2-2
PubMed: 24451478
Affiliations:
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Ellis</name></author><author><name sortKey="Clark, Jennifer" sort="Clark, Jennifer" uniqKey="Clark J" first="Jennifer" last="Clark">Jennifer Clark</name></author><author><name sortKey="Clem, Brian" sort="Clem, Brian" uniqKey="Clem B" first="Brian" last="Clem">Brian Clem</name></author><author><name sortKey="Chesney, Jason" sort="Chesney, Jason" uniqKey="Chesney J" first="Jason" last="Chesney">Jason Chesney</name><affiliation wicri:level="2"><nlm:affiliation>Division of Medical Oncology and Hematology, Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202, USA. jason.chesney@louisville.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Medical Oncology and Hematology, Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202</wicri:regionArea><placeName><region type="state">Kentucky</region></placeName></affiliation></author><author><name sortKey="Telang, Sucheta" sort="Telang, Sucheta" uniqKey="Telang S" first="Sucheta" last="Telang">Sucheta Telang</name></author></analytic><series><title level="j">Cancer & metabolism</title><idno type="ISSN">2049-3002</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Unlike glycolytic enzymes that directly catabolize glucose to pyruvate, the family of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases (PFKFBs) control the conversion of fructose-6-phosphate to and from fructose-2,6-bisphosphate, a key regulator of the glycolytic enzyme phosphofructokinase-1 (PFK-1). One family member, PFKFB3, has been shown to be highly expressed and activated in human cancer cells, and derivatives of a PFKFB3 inhibitor, 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO), are currently being developed in clinical trials. However, the effectiveness of drugs such as 3PO that target energetic pathways is limited by survival pathways that can be activated by reduced ATP and nutrient uptake. One such pathway is the process of cellular self-catabolism termed autophagy. We hypothesized that the functional glucose starvation induced by inhibition of PFKFB3 in tumor cells would induce autophagy as a pro-survival mechanism and that inhibitors of autophagy could increase the anti-tumor effects of PFKFB3 inhibitors.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Kentucky</li></region></list><tree><noCountry><name sortKey="Clark, Jennifer" sort="Clark, Jennifer" uniqKey="Clark J" first="Jennifer" last="Clark">Jennifer Clark</name><name sortKey="Clem, Amy" sort="Clem, Amy" uniqKey="Clem A" first="Amy" last="Clem">Amy Clem</name><name sortKey="Clem, Brian" sort="Clem, Brian" uniqKey="Clem B" first="Brian" last="Clem">Brian Clem</name><name sortKey="Ellis, Steve R" sort="Ellis, Steve R" uniqKey="Ellis S" first="Steve R" last="Ellis">Steve R. Ellis</name><name sortKey="Imbert Fernandez, Yoannis" sort="Imbert Fernandez, Yoannis" uniqKey="Imbert Fernandez Y" first="Yoannis" last="Imbert-Fernandez">Yoannis Imbert-Fernandez</name><name sortKey="Klarer, Alden C" sort="Klarer, Alden C" uniqKey="Klarer A" first="Alden C" last="Klarer">Alden C. Klarer</name><name sortKey="O Neal, Julie" sort="O Neal, Julie" uniqKey="O Neal J" first="Julie" last="O'Neal">Julie O'Neal</name><name sortKey="Telang, Sucheta" sort="Telang, Sucheta" uniqKey="Telang S" first="Sucheta" last="Telang">Sucheta Telang</name></noCountry><country name="États-Unis"><region name="Kentucky"><name sortKey="Chesney, Jason" sort="Chesney, Jason" uniqKey="Chesney J" first="Jason" last="Chesney">Jason Chesney</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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