To gain insights into the role of purinergic receptors in human dental pulp cells (hDPCs) differentiation, we characterized the expression and functional activity of P2Y1 receptors and investigated the effects of ADP on the proliferation and differentiation of this pulp stem-like cell population. Our data showed that ADP did not induce cell proliferation to expose the various ADP concentrations for 72 hours, but the proliferative capacity of hDPCs was inhibited at higher ATP concentrations (100 μM). Using RT-PCR analysis, we found that ADP induced several P2Y receptors including P2Y1 as well as odontoblastic differentiation genes, dentin matrix protein 1 (DMP1) and dentin sialophosphoprotein (DSPP) in a dose-dependent manner. The effects of ADP on the expression of DMP-1 and DSPP mRNA were prevented by the P2Y1 antagonist MRS2179. The extracellular matrix calcium deposits were clearly observed in ADP-treated hDPCs by alizarin red S staining. Quantitative measurement of mineralization induced by ADP was significantly inhibited in MRS2179-treated hDPCs. These results may provide new insights into the molecular regulation of the differentiation of hDPCs.

Multidrug resistance (MDR) remains one of the most significant obstacles in various cancer treatment, and this process often involves dysregulation of the number of micro-RNAs. The aim of this study was to explore the role of miR-4708 on the regulation of MDR-1 expression and the regulation of multidrug resistance (MDR) to chemotherapeutic drugs. Luciferase reporter assays demonstrated that miR-4708 directly binds MDR-1 3’-UTR and down-regulated reporter luciferase activity. The mRNA and protein expression levels of MDR1 were significantly decreased following miR-4708 overexpression. Additionally, the accumulation of rhodamine-123 in paclitacel resistant FaDu cells following miR-4708 transfection was significantly increased compared with control, indicating that the efflux capacity was reduced. These results demonstrated that miR-4708 could be involved in the regulation of MDR via targeting MDR-1 and may provide a potential strategy for reversing drug resistance in oral cancer.