Exploring the crosstalk between long non-coding RNAs and microRNAs to unravel potential prognostic and therapeutic biomarkers in β-thalassemia.

β-thalassemia is a prevalent monogenic disorder characterized by reduced or absent synthesis of the β-globin chain. Although great effort has been made to ameliorate the disease severity of β-thalassemic patients, progress has been stymied due to limited understanding of the detailed molecular mechanism of disease pathogenesis. Recently, non-coding RNAs have been established as key players in regulating various physiological and pathological processes. Many ncRNAs are involved in hematopoiesis and erythroid development. Furthermore, various studies have also reported the complex interplay between different ncRNAs, such as miRNA, lncRNAs, etc. in regulating disease progression and pathogenesis. Both lncRNAs and miRNAs have been identified as independent regulators of globin gene expression and are intricately involved in disease pathogenesis; yet accumulating evidence suggests that the cross-talk between lncRNAs and miRNAs is intricately involved in the underlying globin gene expression, fine-tuning the effect of their independent regulation. In this review, we summarize the current progress of research on the roles of lncRNAs and miRNAs implicated in β-thalassemia disease, including their interactions and regulatory networks. This can provide important insights into the detailed epigenetic regulation of globin gene switching and has the potential to develop novel therapeutic approaches against β-thalassemia.