No abstract

No abstract

No abstract

No abstract

Hepatic fibrosis was one of the causes to hepatocellular cancer (HCC), owing to limited therapeutic options. And hepatocytes can induce liver fibrogenesis via epithelial-mesenchymal transition (EMT). Multiple circRNAs exert critical role in the occurrence of liver fibrosis via working as microRNA (miRNA) sponges. Circ_0072088 is upregulated in hepatocellular cancer (HCC) and promote proliferation, migration of HCC cells. However, the potential research mechanism for circ_0072088 action against the fibrotic progression remain still unknown. The treatment of AML12 hepatocytes with TGF-β1 contributed to dramatically increased in the levels of circ_0072088. Additionally, in terms of mechanism, circ_0072088 was authenticated to function as miR-330-3p sponge, not only noticeable increase EMT, but also induced fibrosis in AML12 hepatocytes. MiR-330-3p could weaken the roles of circ_0072088 acceleration. Moreover, we proved that CDK1, a miR-330-3p target, was time-dependently augmented in the TGF-β1 treated AML12 hepatocytes, and its overexpression weakens the miR-330-3p regulatory effects.Our findings provided a unique role of the circ_0072088 mediates hepatic fibrosis renders epithelial-mesenchymal transition at least partially through miR-330-3p/CDK1 axis, thus suggesting its tremendous therapeutic potential in the treatment of liver diseases.