ERBB2 and breast carcinoma: Further studies revealed that entinostat induced expression of miR-125a, miR-125b, and miR-205, all of which were reported to directly target the 3’UTR of erbB3 mRNA [35, 36], and the three miRNAs acted in concert to inhibit HER3 protein translation in HER2-overexpressing breast cancer cells [27].