Finally, our in vivo experiment demonstrated that lentivirus-mediated delivery of miR-20a promoted tumor growth in murine xenograft model of MM, which provide evidence that miR-20a inhibitor exerts therapeutic activity in preclinical models and supports a framework for the development of miR-19b/20a-based treatment strategies for MM patients.
Furthermore, to accurately predict the optimal target genes of MM, the logFC, targetScanCS and targetScanPCT values of known genes in four miRNAs (i.e. has-miR-21, has-miR-20a, has-miR-148a and has-miR-99b) were used to compute the targetScore values.
Furthermore, we observed decreased expression of miR-93 and miR-20a in MM-MSCs, while upregulation of miR-93/miR-20a decreased cellular senescence, as evidenced by the increased p21 expression.
Our findings suggest that miR-181a/20a has a higher expression in MM. miR-181-a expression is proportional to MM tumor burden and could be a biomaker for monitoring treatment. miR-20a shows the potential of a diagnostic biomarker.
Finally, the drug significantly down-modulated the MIRHG1 transcript and its associated microRNA, miR-19a and miR-19b, known to have oncogenic activity in multiple myeloma.