1- Department of Medical Laboratory Sciences, School of Paramedical Sciences, Arak University of Medical Sciences, Arak, Iran
2- Department of Hematology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran , s.hassani@arakmu.ac.ir
Abstract: (29 Views)
Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy characterized by poor prognosis and limited overall survival, particularly in older patients. Despite significant progress in chemotherapy, molecular diagnostics, and supportive care, resistance to apoptosis remains a central obstacle in AML treatment. Long non-coding RNAs (lncRNAs), a subgroup of non-coding RNAs (ncRNAs), have recently gained attention as critical regulators of gene expression and cellular functions, including proliferation, differentiation, apoptosis, and drug resistance. Through the competing endogenous RNA (ceRNA) mechanism, lncRNAs act as molecular sponges for microRNAs, thereby modulating the expression of apoptosis-related genes. In this review, we comprehensively summarize and analyze current evidence regarding the roles of lncRNAs in regulating apoptosis in AML cells. Recent findings demonstrate that certain lncRNAs, such as HOTAIR, UCA1, TUG1, and H19, promote leukemic progression by suppressing apoptosis, while others, including NEAT1 and DUXAP8, enhance apoptosis and may function as tumor suppressors. Dysregulation of lncRNAs not only contributes to malignant transformation and therapeutic resistance but also correlates with patient outcomes. By integrating available studies, our review highlights the dual functions of lncRNAs in AML pathogenesis and emphasizes their potential as prognostic biomarkers and therapeutic targets, providing insights that may guide future translational and clinical research.
Type of Study:
Review Article |
Subject:
Oncology Received: 2023/03/26 | Accepted: 2025/10/4