The ability to convert somatic cells to a different developmental lineage holds great promise for cell-based therapy. The field of direct cell lineage reprogramming has undergone rapid development in recent years. It is now possible to directly convert fully differentiated mature somatic cells into other cell types while bypassing an intermediate pluripotent state. Thus, recent advances in this field has opened up the possibility for the development of patient-specific therapies, and are thus a great leap forward in translational regenerative medicine.

 

Recent studies show that microRNAs can promote cell reprogramming and mostly acting as an upstream regulator of different transcription factors. MicroRNAs (miRNAs) are a class of short non-coding RNAs, about 19–22 nucleotides in length that can bind to complementary target sites in mRNA molecules causing translation repression or the cleavage of the target mRNAs. MicroRNA are expressed in all higher eukaryotes, and a recent estimate suggests that up to 60% of human genes may be subjected to microRNA control. The repressive actions of miRNAs on gene expression can be powerful as a single miRNA may target multiple pathways simultaneously. Taking into consideration that miRNAs have the potential to be used as small-molecule therapeutics for cellular reprogramming, recent findings in this direction open new possibilities for direct reprogramming of cells into other cell lineages.

 

Our laboratory is focused to understand the role of miRNAs and other non-coding RNAs in cellular lineage conversion which can be effectively used for therapeutics against cancer and diabetes. Changing of cellular fate and its physiology is a key plank for the onset of disease development and progression, however, the cellular and molecular mechanism of such event is not yet explored. We therefore interested to investigate the underlying molecular mechanism of fibroblast to endothelial transdifferentiation, white to brown/beige adipocyte conversion and macrophage proinflammatory M1 to anti-inflammatory M2 phenotype polarization and the involvement of miRNAs and other non-coding RNAs therein.