Evaluation of MicroRNA as Minimal Residual Disease in  Leukemia: Diagnostic and Prognostic Approach: A Review

Bahareh Shateri  Amiri; Neda  Sabernia; Behdokht  Abouali; Parya  Amini; Hadi  Rezaeeyan

doi:10.18502/ijph.v52i12.14315

Bahareh Shateri Amiri Department of Internal Medicine, School of Medicine, Hazrat-e Rasool General Hospital, Iran University of Medical Sciences Teh-ran, Iran
Neda Sabernia Department of Internal Medicine, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
Behdokht Abouali Department of Ophthalmology, School of Medicine, Infectious Ophthalmologic Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Parya Amini Department of Cardiology, School of Medicine, Ahvaz Jundishapur University of Medical Science, Ahvaz, Iran
Hadi Rezaeeyan Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Iranian Blood Transfu-sion Organization, Tehran, Iran

DOI: https://doi.org/10.18502/ijph.v52i12.14315

Keywords: MicroRNAs; Minimal residual disease; Pathogenesis; Prognosis; Diagnosis

Abstract

Various factors are effective in the development of minimal residual disease (MRD), one of which is MicroRNAsmiRNAs miRNAs and their dysfunction in gene expression have influential role in the pathogenesis of leukemia. Nowadays, treatments that lead to the suppression or replacement of miRNAs have been developed. Focusing on the role of miRNAs in managing the treatment of leukemia, in this review article we have investigated the miRNAs and signaling pathways involved in the process of apoptosis and cell proliferation, as well as miRNAs with oncogenic function in malignant leukemia cells. Among the studied miRNAs, miR-99a, and miR-181a play an essential role in apoptosis, proliferation and oncogenesis via AKT, MAPK, RAS, and mTOR signaling pathways. miR-223 and miR-125a affect apoptosis and oncogenesis via Wnt/B-catenin, PTEN/PI3K, and STAT5/AKT/ERK/Src signaling pathways. miR-100 also affects both apoptosis and oncogenesis; it acts via IGF1 and mTOR signaling pathways.