Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/235563
Type: Artigo de periódico
Title: Differential Profile Of Pip4k2a Expression In Hematological Malignancies.
Author: Lima, Keli
Ribeiro, Daniela Maria
Campos, Paula de Melo
Costa, Fernando Ferreira
Traina, Fabiola
Saad, Sara Teresinha Olalla
Sonati, Maria de Fátima
Machado-Neto, João Agostinho
Abstract: PIP4K2A is a lipid kinase that phosphorylates PtdIns5P, generating PtdIns4,5P2. Recently, PIP4K2A was identified as a potential target in acute myeloid leukemia cells. The objective of the present study was to investigate the PIP4K2A expression in hematological malignancies and verify the effects of PIP4K2A silencing on proliferation and survival of leukemia cell lines. PIP4K2A was found to be a cytoplasmic and nuclear protein with reduced levels in leukemia cell lines compared to normal leukocytes. PIP4K2A mRNA levels were significantly reduced in bone marrow cells from acute lymphoid leukemia (ALL) patients compared with healthy donors and in myelodysplastic syndromes (MDS) with ≥5% compared with <5% bone marrow blasts. Low PIP4K2A expression (lowest tertile versus 2 higher tertiles) negatively impacted overall survival of MDS patients by univariate analysis. PIP4K2A silencing did not modulate cell proliferation, clonogenicity and apoptosis of HEL and Namalwa leukemia cells. In summary, we characterized the expression of PIP4K2A in a cohort of patients with hematological malignancies and we found that PIP4K2A mRNA expression is downregulated in RAEB-1/RAEB-2 MDS and ALL cells, and PIP4K2A silencing does not modulate cell survival in HEL and Namalwa leukemia cells.
Subject: Alpha
Cell Viability
Leukemia
Myelodysplastic Syndromes
Pip4k2a
Phosphatidylinositol
Phosphatidylinositol-5-phosphate 4-kinase
Type Ii
Citation: Blood Cells, Molecules & Diseases. v. 55, n. 3, p. 228-235, 2015-Oct.
Rights: embargo
Identifier DOI: 10.1016/j.bcmd.2015.06.014
Address: http://www.ncbi.nlm.nih.gov/pubmed/?term=26227852
Date Issue: 2015
Appears in Collections:Unicamp - Artigos e Outros Documentos

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