https://www.selleckchem.com/pr....oducts/mizagliflozin
Moreover, miR-137 targeted directly and inhibited DNMT3a in HCC cells, which further retarded cell proliferative, migratory and invasive capabilities, while promoted apoptotic ones. Additionally, miR-137 overexpression inactivated the PTEN/Akt pathway in HCC cell by decreasing DNMT3a expression. Furthermore, miR-137 overexpression inhibited tumor growth in vivo in HCC via interacting with DNMT3a through inhibiting the PTEN/Akt cascades. Our findings suggested that miR-137 inhibited HCC tumor growth and progression via interacting