MicroRNA expression and activity in T-cell acute lymphoblastic leukemia

Fang Ye

doi:10.18632/oncotarget.23539

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is a lymphoid malignancy caused by the oncogenic transformation of immature T-cell progenitors. Many biologically relevant genetic and epigenetic alterations have been identified as driving factors for this transformation. Recently, microRNAs (miRNAs) have been shown to influence various leukemias, including T-ALL. Aberrant expression of miRNAs can function as either oncogenes or tumor suppressors in T-ALL through the regulation of cell migration, invasion, proliferation, apoptosis, and chemoresistance. This occurs by targeting key signaling pathways or transcriptional factors that play a critical role in T-ALL pathology and progression. Different miRNA expression profiles have been linked to specific genetic subtypes of human T-ALL. Furthermore, miRNAs can also act as independent prognostic factors to predict clinical outcomes for T-ALL patients. In the current review, we will focus on the role of miRNAs in the development and progression of T-ALL.

Highlights

T-cell acute lymphoblastic leukemia (T-ALL) is a lymphoid malignancy caused by oncogenic transformation of immature T-cell progenitors [1]
A number of key signaling pathways that play critical role in T-ALL pathology and progression are involved in the miRNA regulatory network including the NOTCH pathway, whose aberrant constitutive activation is believed to be the predominant oncogenic event in the pathogenesis of T-ALL [13]
MiRNA expression profiles, target prediction algorithms of miRNAs, and key protein-coding genes known to be involved in T-ALL, as well as functional studies have created a complicated co-regulatory network that eventually influence leukemia pathogenesis, progression, treatment, and prognosis (Table 1)

Summary

Introduction

T-cell acute lymphoblastic leukemia (T-ALL) is a lymphoid malignancy caused by oncogenic transformation of immature T-cell progenitors [1]. Aberrant expression of miRNAs can function as either oncogenes or tumor suppressors in T-ALL through the regulation of cell migration, invasion, proliferation, apoptosis, and chemoresistance. Together these result in the aberrant expression of various T-cell fate specific and thymocyte development related transcription factors and epigenetic regulators that can become oncogenes or tumor suppressors.

Results

Conclusion