Hepatocytic stem cells (HSCs) have inhibitory effects on hepatocarcinoma cells. The present study investigated the effects of HSC activity in hepatocarcinoma cells . A Transwell co-culture system of hepatocytic precursor (stem-like) WB-F344 cells and hepatoma CBRH-7919 cells was used to assess HSC activity in metastasized hepatoma cells . Nude mouse xenografts were used to assess HSC activity . Co-culture of hepatoma CBRH-7919 cells with WB-F344 cells suppressed the growth and colony formation, tumor cell migration and invasion capacity of CBRH-7919 cells. The nude mouse xenograft assay demonstrated that the xenograft size of CBRH-7919 cells following co-culture with WB-F344 cells was significantly smaller compared with that of control cells. Furthermore, the expression levels of the epithelial markers E-cadherin and β-catenin were downregulated, while the mesenchymal markers α-SMA and vimentin were upregulated. Co-culture of CBRH-7919 cells with WB-F344 cells downregulated NF-κB and phospho-Akt expression. In conclusion, hepatocytic precursor (stem-like) WB-F344 cells inhibited the growth, colony formation and invasion capacity of metastasized hepatoma CBRH-7919 cells and by downregulating Akt/NF-κB signaling.
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http://dx.doi.org/10.3892/ol.2016.5128 | DOI Listing |
J Cell Commun Signal
December 2023
College of Life Sciences, State Key Laboratory Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Pulmonary Fibrosis, Institute of Biomedical Science, Henan Normal University, Henan Xinxiang, 453007, China.
G protein-coupled receptors (GPCRs) play important roles in tumorigenesis and the development of hepatocellular carcinoma (HCC). GPR50 is an orphan GPCR. Previous studies have indicated that GPR50 could protect against breast cancer development and decrease tumor growth in a xenograft mouse model.
View Article and Find Full Text PDFMol Cell Endocrinol
April 2022
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, China; Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education of China, Beijing, China. Electronic address:
Background: Nonalcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in hepatocytes. The involvement of programmed cell death 4 (Pdcd4) in inflammation and metabolic diseases has been widely reported. However, the precise regulatory role of Pdcd4 in hepatocytic lipid metabolism and NAFLD is not well known.
View Article and Find Full Text PDFJ Oncol
January 2021
Gene Engineering Drug and Biotechnology Beijing Key Laboratory, Department of Biochemistry and Molecular Biology, College of Life Sciences, Beijing Normal University, Beijing 100875, China.
Urine can accumulate systemic changes with no mechanism to be stable, which may reflect early changes associated with physiological or pathophysiological processes. To explore the potential value of the urine proteome, two rat models were established by intrahepatic injection of two different hepatoma cell lines, CBRH-7919 and RH-35. Urine samples were collected and analyzed.
View Article and Find Full Text PDFBioorg Med Chem Lett
September 2017
Division of Endocrinology, Metabolism and Molecular Medicine, Charles R. Drew University of Medicine and Sciences, UCLA School of Medicine, Los Angeles, CA, USA.
Extensive studies have been performed on the role of 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) in metabolic diseases. Our previous study reported glucose could directly regulate hexose-6-phosphate dehydrogenase (H6PDH) and 11β-HSD1. Recently, we further investigated the interplay of H6PDH and 11β-HSD1 and their roles in hepatic gluconeogenesis and insulin resistance to elucidate the importance of H6PDH and 11β-HSD1 in pathogenesis of type 2 diabetes mellitus (T2DM).
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