Long non-coding RNAs regulate treatment outcome in leukemia: What have we learnt recently?

Leukemia is a group of highly heterogeneous and life-threatening blood cancers that originate from abnormal hematopoietic stem cells. Multiple treatments are approved for leukemia, including chemotherapy, targeted therapy, hematopoietic stem cell transplantation, radiation therapy, and immunotherapy. Unfortunately, therapeutic resistance occurs in a substantial proportion of patients and greatly compromises the treatment efficacy of leukemia, resulting in relapse and mortality. The abnormal activity of receptor tyrosine kinases, cell membrane transporters, intracellular signal transducers, transcription factors, and anti-apoptotic proteins have been shown to contribute to the emergence of therapeutic resistance. Despite these findings, the exact mechanisms of treatment resistance are still not fully understood, which limits the development of effective measures to overcome it. Long non-coding RNAs (lncRNA) are a class of regulatory molecules that are gaining increasing attention, and lncRNA-mediated regulation of therapeutic resistance against multiple drugs for leukemia is being revealed. These dysregulated lncRNAs not only serve as potential targets to reduce resistance but also might improve treatment response prediction and individualized treatment decision. Here, we summarize the recent findings on lncRNA-mediated regulation of therapeutic resistance in leukemia and discuss future perspectives on how to make use of the dysregulated lncRNAs in leukemia to improve treatment outcome.