Investigating autophagy and miRNAs as therapeutic targets in leukemia

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Abstract
Leukemia, characterized by the uncontrolled proliferation of abnormal white blood cells, encompasses several subtypes, including acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL), and chronic myeloid leukemia (CML). It presents a significant challenge in treatment due to its complex biology and the presence of drug resistance. Autophagy, a cellular process responsible for degrading and recycling cellular components, plays a dual role in leukemia. On one hand, autophagy helps cancer cells survive and adapt to stressors, including chemotherapy, promoting drug resistance. On the other hand, it can also function as a tumor suppressor by enhancing sensitivity to treatment. MicroRNAs (miRNAs), small RNA molecules that regulate gene expression, are crucial in modulating autophagy-related genes and signaling pathways in leukemia. Dysregulated miRNAs can either inhibit or enhance autophagy, influencing leukemia progression and response to therapy. Targeting the interaction between autophagy and miRNAs presents a novel therapeutic strategy to overcome drug resistance and improve leukemia treatment outcomes. By understanding the molecular mechanisms of autophagy and miRNAs, new treatment strategies could be developed that focus on restoring proper autophagic function and miRNA regulation, ultimately enhancing the effectiveness of chemotherapy and reducing side effects. This review explores the dual roles of autophagy and miRNAs in leukemia, providing a deeper insight into their interplay and their potential for improving therapeutic approaches. Graphical Abstract

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