Retinoid receptor signaling and autophagy in acute promyelocytic leukemia.

Hdl Handle:
http://hdl.handle.net/10147/322508
Title:
Retinoid receptor signaling and autophagy in acute promyelocytic leukemia.
Authors:
Orfali, Nina; McKenna, Sharon L; Cahill, Mary R; Gudas, Lorraine J; Mongan, Nigel P
Affiliation:
Cork Cancer Research Center, University College Cork, Cork, Ireland; Department of Pharmacology, Weill Cornell Medical College, New York, NY 10065, USA.
Citation:
Retinoid receptor signaling and autophagy in acute promyelocytic leukemia. 2014, 324 (1):1-12 Exp. Cell Res.
Journal:
Experimental cell research
Issue Date:
15-May-2014
URI:
http://hdl.handle.net/10147/322508
DOI:
10.1016/j.yexcr.2014.03.018
PubMed ID:
24694321
Abstract:
Retinoids are a family of signaling molecules derived from vitamin A with well established roles in cellular differentiation. Physiologically active retinoids mediate transcriptional effects on cells through interactions with retinoic acid (RARs) and retinoid-X (RXR) receptors. Chromosomal translocations involving the RARα gene, which lead to impaired retinoid signaling, are implicated in acute promyelocytic leukemia (APL). All-trans-retinoic acid (ATRA), alone and in combination with arsenic trioxide (ATO), restores differentiation in APL cells and promotes degradation of the abnormal oncogenic fusion protein through several proteolytic mechanisms. RARα fusion-protein elimination is emerging as critical to obtaining sustained remission and long-term cure in APL. Autophagy is a degradative cellular pathway involved in protein turnover. Both ATRA and ATO also induce autophagy in APL cells. Enhancing autophagy may therefore be of therapeutic benefit in resistant APL and could broaden the application of differentiation therapy to other cancers. Here we discuss retinoid signaling in hematopoiesis, leukemogenesis, and APL treatment. We highlight autophagy as a potential important regulator in anti-leukemic strategies.
Item Type:
Article
Language:
en
MeSH:
Animals; Autophagy; Cell Differentiation; Hematopoiesis; Humans; Leukemia, Promyelocytic, Acute; Receptors, Retinoic Acid; Retinoids; Signal Transduction
ISSN:
1090-2422

Full metadata record

DC FieldValue Language
dc.contributor.authorOrfali, Ninaen_GB
dc.contributor.authorMcKenna, Sharon Len_GB
dc.contributor.authorCahill, Mary Ren_GB
dc.contributor.authorGudas, Lorraine Jen_GB
dc.contributor.authorMongan, Nigel Pen_GB
dc.date.accessioned2014-07-07T09:18:43Z-
dc.date.available2014-07-07T09:18:43Z-
dc.date.issued2014-05-15-
dc.identifier.citationRetinoid receptor signaling and autophagy in acute promyelocytic leukemia. 2014, 324 (1):1-12 Exp. Cell Res.en_GB
dc.identifier.issn1090-2422-
dc.identifier.pmid24694321-
dc.identifier.doi10.1016/j.yexcr.2014.03.018-
dc.identifier.urihttp://hdl.handle.net/10147/322508-
dc.description.abstractRetinoids are a family of signaling molecules derived from vitamin A with well established roles in cellular differentiation. Physiologically active retinoids mediate transcriptional effects on cells through interactions with retinoic acid (RARs) and retinoid-X (RXR) receptors. Chromosomal translocations involving the RARα gene, which lead to impaired retinoid signaling, are implicated in acute promyelocytic leukemia (APL). All-trans-retinoic acid (ATRA), alone and in combination with arsenic trioxide (ATO), restores differentiation in APL cells and promotes degradation of the abnormal oncogenic fusion protein through several proteolytic mechanisms. RARα fusion-protein elimination is emerging as critical to obtaining sustained remission and long-term cure in APL. Autophagy is a degradative cellular pathway involved in protein turnover. Both ATRA and ATO also induce autophagy in APL cells. Enhancing autophagy may therefore be of therapeutic benefit in resistant APL and could broaden the application of differentiation therapy to other cancers. Here we discuss retinoid signaling in hematopoiesis, leukemogenesis, and APL treatment. We highlight autophagy as a potential important regulator in anti-leukemic strategies.en_GB
dc.language.isoenen
dc.rightsArchived with thanks to Experimental cell researchen_GB
dc.subject.meshAnimals-
dc.subject.meshAutophagy-
dc.subject.meshCell Differentiation-
dc.subject.meshHematopoiesis-
dc.subject.meshHumans-
dc.subject.meshLeukemia, Promyelocytic, Acute-
dc.subject.meshReceptors, Retinoic Acid-
dc.subject.meshRetinoids-
dc.subject.meshSignal Transduction-
dc.titleRetinoid receptor signaling and autophagy in acute promyelocytic leukemia.en_GB
dc.typeArticleen
dc.contributor.departmentCork Cancer Research Center, University College Cork, Cork, Ireland; Department of Pharmacology, Weill Cornell Medical College, New York, NY 10065, USA.en_GB
dc.identifier.journalExperimental cell researchen_GB
dc.description.fundingNo fundingen
dc.description.provinceMunsteren
dc.description.peer-reviewpeer-reviewen

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