Dissecting chronic lymphocytic leukemia microenvironment signals in patients with unmutated disease: MicroRNA-22 regulates phosphatase and tensin homolog/AKT/FOXO1 pathway in proliferative leukemic cells

Florencia Palacios, Daniel Prieto, Cecilia Abreu, Santiago Ruiz, Pablo Morande, Tamara Fernández-Calero, Gabriela Libisch, Ana Inés Landoni, Pablo Oppezzo*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

12 Citations (Scopus)

Abstract

Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of clonal B cells arrested in G0/G1 stages that coexist with proliferative B cells. We identified one of these proliferative subsets in the peripheral blood from patients with unmutated disease (UM). Aiming to characterize the molecular mechanism underlying this proliferative behavior, we performed gene expression analysis of the mRNA and microRNAs in this leukemic subpopulation and compared results with those for the quiescent counterpart. Our results suggest that proliferation of this subset mainly depends on microRNA-22 overexpression, which induces phosphatase and tensin homolog (PTEN) down-regulation and phosphoinositide 3-kinase (PI3K)/AKT pathway activation. These results underline the role of the PI3K/AKT pathway at the origin of this proliferative pool in patients with UM CLL and provide additional rationale for the use of PI3K inhibitors.

Original languageEnglish
Pages (from-to)1560-1565
Number of pages6
JournalLeukemia and Lymphoma
Volume56
Issue number5
DOIs
Publication statusPublished - 1 May 2015
Externally publishedYes

Keywords

  • CLL microenvironment signals
  • Unmutated patients

Fingerprint

Dive into the research topics of 'Dissecting chronic lymphocytic leukemia microenvironment signals in patients with unmutated disease: MicroRNA-22 regulates phosphatase and tensin homolog/AKT/FOXO1 pathway in proliferative leukemic cells'. Together they form a unique fingerprint.

Cite this