Analysis of the expression and prognostic significance of DDK complex in Hepatocarcinoma.

Background: Hepatocellular carcinoma (HCC) remains one of the most common and lethal malignancies worldwide. Although DBF4-dependent kinase (DDK) complex composed of CDC7 kinase and its regulatory subunit DBF4 has been shown to be overexpressed in primary tumors and promotes tumor development, while its role and prognostic value in HCC remain largely unknown. In the present study, the expression of DBF4 and CDC7 and their relationship with clinical characteristics were comprehensively analyzed.

Histone deacetylase 3 promotes liver regeneration and liver cancer cells proliferation through signal transducer and activator of transcription 3 signaling pathway.

Histone deacetylase 3 (HDAC3) plays pivotal roles in cell cycle regulation and is often aberrantly expressed in various cancers including hepatocellular carcinoma (HCC), but little is known about its role in liver regeneration and liver cancer cells proliferation. Using an inducible hepatocyte-selective HDAC3 knockout mouse, we find that lack of HDAC3 dramatically impaired liver regeneration and blocked hepatocyte proliferation in the G1 phase entry. HDAC3 inactivation robustly disrupted the signal transducer and activator of transcription 3 (STAT3) cascade.

Elevated expression of Gα in intrahepatic cholangiocarcinoma associates with poor prognosis.

Background: The stimulatory G protein a subunit (Gα) plays important roles in diverse cell processes including tumorigenesis. Activating mutations in Gα gene (GNAS) have been reported to be associated with poor prognosis in various human carcinomas. Furthermore, Gα signaling is crucial in promoting liver regeneration by interacting with growth factor signaling, indicating that Gα might play a promoting role in cancer development.

Loss of Dicer1 impairs hepatocyte survival and leads to chronic inflammation and progenitor cell activation.

Aim: To investigate the continuous hepatic histopathological processes which occur in response to the loss of Dicer1.

Methods: We generated a hepatocyte-selective Dicer1 knockout mouse and observed the gradual hepatic histopathological changes in the mutant liver. Immunohistochemistry and Western blotting were performed to detect Dicer1 expression.