MiR-30 family and EMT in human fetal pancreatic islets

Small, non-coding ribonucleotides called micro RNAs (miRNAs) have recently emerged as important regulators of cell function. MiRNAs regulate gene expression mainly by binding to the 3' UTR of mRNAs and thereby inhibit the translation of target mRNAs. The abundance of many miRNAs is altered under physiological and pathophysiological conditions, such as cancer and neurodegeneration. Recent data suggest that miRNAs also have an important role in regulation of insulin gene transcription, insulin secretion, and pancreatic islet cell function. An interesting study by Joglekar et al. published in this issue of ISLETS suggests that the miR-30 family of miRNAs may control the epithelial-to-mesenchymal transition of primary cultures of human pancreatic epithelial cells by negatively regulating the translation of mesenchymal gene transcripts such as vimentin. These findings are in agreement with previous data that suggest an important role for one of the miR-30 family members (miR-30d) in insulin gene expression in pancreatic beta cells. In summary, the report by Joglekar et al provides a significant advancement in understanding the role of miRNAs in pancreatic islet development and suggests that manipulation of miR-30 family of miRNA expression may provide an important means to generate and expand pancreatic beta cells from human fetal pancreatic progenitors.