Nuclear inositide signaling in myelodysplastic syndromes.
Myelodysplastic syndromes (MDS) are defined as clonal hematopoietic stem-cell disorders characterized by ineffective hematopoiesis in one or more of the lineages of the bone marrow. Although distinct morphologic subgroups exist, the natural history of MDS is progression to acute myeloid leukemia (AML). However, the molecular the mechanisms the underlying MDS evolution to AML are not completely understood. Inositides are key cellular second messengers with well-established roles in signal transduction pathways, and nuclear metabolism elicited by phosphoinositide-specific phospholipase C (PI-PLC) beta1 and Akt plays an important role in the control of the balance between cell cycle progression and apoptosis in both normal and pathologic conditions. Recent findings evidenced the role played by nuclear lipid signaling pathways, which could become promising therapeutic targets in MDS. This review will provide a concise and updated revision of the state of art on this topic.
Follo
Matilde Y
MY
Cellular Signaling Laboratory, Department of Human Anatomical Sciences, University of Bologna, via Irnerio 48, 40126 Bologna, Italy.
Mongiorgi
Sara
S
Finelli
Carlo
C
Clissa
Cristina
C
Ramazzotti
Giulia
G
Fiume
Roberta
R
Faenza
Irene
I
Manzoli
Lucia
L
Martelli
Alberto M
AM
Cocco
Lucio
L
D000818:Animals; D002467:Cell Nucleus / Q000378:metabolism*; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000378:metabolism / Q000473:pathology; D009190:Myelodysplastic Syndromes / Q000378:metabolism* / Q000503:physiopathology; D010716:Phosphatidylinositols / Q000378:metabolism; D054799:Phospholipase C beta / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*
D010716:Phosphatidylinositols; D051057:Proto-Oncogene Proteins c-akt; D054799:Phospholipase C beta