Interplay between LncRNAs and autophagy-related pathways in leukemia: mechanisms and clinical implications.

Abstract

Autophagy is a conserved catabolic process that removes protein clumps and defective organelles, thereby promoting cell equilibrium. Growing data suggest that dysregulation of the autophagic pathway is linked to several cancer hallmarks. Long non-coding RNAs (lncRNAs), which are key parts of gene transcription, are increasingly recognized for their significant roles in various biological processes. Recent studies have uncovered a strong connection between the mutational landscape and altered expression of lncRNAs in the tumor formation and development, including leukemia. Research over the past few years has emphasized the role of lncRNAs as important regulators of autophagy-related gene expression. These RNAs can influence key leukemia characteristics, such as apoptosis, proliferation, epithelial-mesenchymal transition (EMT), migration, and angiogenesis, by modulating autophagy-associated signaling pathways. With altered lncRNA expression observed in leukemia cells and tissues, they hold promise as diagnostic biomarkers and therapeutic targets. The current review focuses on the regulatory function of lncRNAs in autophagy and their involvement in leukemia, potentially uncovering valuable therapeutic targets for leukemia treatment.