Title:
Expression analysis of mir-17-5p, mir-20a and let-7a microRNAs and their target proteins in CD34+ bone marrow cells of patients with myelodysplastic syndromes
Languages of Item:
English
Abstract:
Mir-17-5p and mir-20a, members of the mir-17-92 family, down-regulate E2F1, which is over-expressed in myelodysplastic syndromes (MDS). Moreover, let-7a down-regulates KRAS, which is aberrantly expressed in MDS. We evaluated the expression of the aforementioned microRNAs in CD34+ cells of 43 MDS patients using real-time PCR and their target proteins (E2F1, MYC, BCL2, CCND1, and KRAS) by Western blot. Mir-17-5p and mir-20a were under expressed in high risk MDS patients, compared to low risk MDS patients. Similarly, let-7a was under expressed in patients with intermediate or high-risk karyotype. Interestingly, there was an inverse correlation between microRNA and the expression levels of their targets. Importantly, mir-17-5p and mir-20a constitute favorable prognostic factors in MDS, since their expression was associated with increased overall survival of MDS patients. © 2012 Elsevier Ltd.
Authors:
Vasilatou, D.
Papageorgiou, S.G.
Kontsioti, F.
Kontos, C.K.
Tsiotra, P.
Mpakou, V.
Pavlou, M.A.S.
Economopoulou, C.
Dimitriadis, G.
Dervenoulas, J.
Pappa, V.
Journal:
Leukemia Research
Keywords:
cyclin D1; K ras protein; microRNA; microRNA 17 5p; microRNA 20a; microRNA let 7a; Myc protein; protein bcl 2; transcription factor E2F1; unclassified drug, adult; article; bone marrow cell; CD34 selection; clinical article; controlled study; cytogenetics; down regulation; female; high risk patient; human; human cell; karyotype; low risk population; male; myelodysplastic syndrome; overall survival; priority journal; prognosis; protein expression; protein targeting; real time polymerase chain reaction; Western blotting, Aged; Aged, 80 and over; Antigens, CD34; Bone Marrow Cells; Case-Control Studies; Female; Gene Expression Profiling; Gene Expression Regulation; Humans; Male; MicroRNAs; Middle Aged; Myelodysplastic Syndromes; Prognosis
Official URL (Publisher):
DOI:
10.1016/j.leukres.2012.11.011
