Directed differentiation of human pluripotent stem cells into pancreatobiliary co-progenitor-like population.

Progress in uncovering the causes of extrahepatic biliary diseases and developing new therapies has been constrained by the inaccessibility of donor tissue and a lack of experimental models. Although hepatic, intrahepatic biliary, and pancreatic 2D/3D models have been successfully established from pluripotent stem cells (PSCs), in vitro generation of extrahepatic biliary cells remains a major challenge, due to the absence of developmental cues. Here we report a de novo method for directed differentiation of human PSCs (both embryonic and induced) into pancreato-biliary progenitors-like cells (PBPLCs).

Integrated Bioinformatics Analysis and Validation of the Prognostic Value of Expression in Hepatocellular Carcinoma.

Background: s function in hepatocellular carcinoma (HCC) has rarely been addressed. We intend to explore the prognostic significance and therapeutic meaning of in HCC in this study.

Methods: Multiple common databases were integrated to analyze the expression status and prognostic meaning of in HCC.

Aldehyde dehydrogenase-2 (ALDH2) opposes hepatocellular carcinoma progression by regulating AMP-activated protein kinase signaling in mice.

Unlabelled: Potential biomarkers that can be used to determine prognosis and perform targeted therapies are urgently needed to treat patients with hepatocellular carcinoma (HCC). To meet this need, we performed a screen to identify functional genes associated with hepatocellular carcinogenesis and its progression at the transcriptome and proteome levels. We identified aldehyde dedydrogenase-2 (ALDH2) as a gene of interest for further study.

CYP3A5 Functions as a Tumor Suppressor in Hepatocellular Carcinoma by Regulating mTORC2/Akt Signaling.

CYP3A5 is a cytochrome P450 protein that functions in the liver metabolism of many carcinogens and cancer drugs. However, it has not been thought to directly affect cancer progression. In this study, we challenge this perspective by demonstrating that CYP3A5 is downregulated in many hepatocellular carcinomas (HCC), where it has an important role as a tumor suppressor that antagonizes the malignant phenotype.

MUC15 inhibits dimerization of EGFR and PI3K-AKT signaling and is associated with aggressive hepatocellular carcinomas in patients.

Background & Aims: Aberrant expression of MUC15 correlates with development of colorectal adenocarcinoma, and MUC15 has been reported to prevent trophoblast invasion of human placenta. However, little is known about the role of MUC15 in pathogenesis of hepatocellular carcinoma (HCC).

Methods: We analyzed HCC samples and matched nontumor liver tissues (controls) collected from 313 patients who underwent hepatectomy in Shanghai, China, from January 2006 through September 2009.