title: Cell expression patterns of CD147 in N-diethylnitrosamine/phenobarbital-induced mouse hepatocellular carcinoma.
abstract: Overexpression of CD147/basigin in hepatic cells promotes the progression of hepatocellular carcinoma (HCC). Whether CD147 also expressed in liver non-parenchymal cells and associated with HCC development was unknown. The aim of the study was to explore time-dependent cell expression patterns of CD147 in a widely accepted N-diethylnitrosamine/phenobarbital (DEN/PB)-induced HCC mouse model. Liver samples collected at month 1-12 of post-DEN/PB administration were assessed the localization of CD147 in hepatocytes, endothelial cells, hepatic stellate cells, and macrophages. Immunohistochemistry analysis showed that CD147 was upregulated in liver tumors during month 1-8 of DEN/PB induction. Expression of CD147 was positively correlated with cytokeratin 18, a hepatocyte marker (r = 0.7857, P = 0.0279), CD31 (r = 0.9048, P = 0.0046), an endothelial cell marker, and CD68, a macrophage marker (r = 0.7619, P = 0.0368). A significant correlation was also observed between CD147 and alpha-smooth muscle actin (r = 0.8857, P = 0.0333) at DEN/PB initiation and early stage of tumor formation. Immunofluorescence and fluorescence in situ hybridization showed that CD147 co-expressed with cytokeratin 18, CD31, alpha-smooth muscle actin, and CD68. Moreover, there existed positive correlations between CD147 and microvessel density (r = 0.7857, P = 0.0279), CD147 and Ki-67 (r = 0.9341, P = 0.0022) in the development of DEN/PB-induced HCC. In conclusion, our results demonstrated that CD147 was upregulated in the liver parenchymal and mesenchymal cells and involved in angiogenesis and tumor cell proliferation in the development of DEN/PB-induced HCC.
authors.affiliation: Cell Engineering Research Center and Department of Cell Biology, State Key Laboratory of Cancer Biology, Fourth Military Medical University, No. 169, Changle West Road, Xi'an, 710032, China.
authors.forename: Meng
authors.initials: M
authors.lastname: Lu
authors.forename: Jiao
authors.initials: J
authors.lastname: Wu
authors.forename: Feng
authors.initials: F
authors.lastname: He
authors.forename: Xi-Long
authors.initials: XL
authors.lastname: Wang
authors.forename: Can
authors.initials: C
authors.lastname: Li
authors.forename: Zhi-Nan
authors.initials: ZN
authors.lastname: Chen
authors.forename: Huijie
authors.initials: H
authors.lastname: Bian
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D051926:Basigin / Q000235:genetics / Q000378:metabolism*; D002273:Carcinogens; D006528:Carcinoma, Hepatocellular / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D049109:Cell Proliferation; D004052:Diethylnitrosamine / Q000009:adverse effects; D015870:Gene Expression; D055166:Hepatic Stellate Cells / Q000378:metabolism; D007150:Immunohistochemistry; D008113:Liver Neoplasms / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D008114:Liver Neoplasms, Experimental / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D008297:Male; D051379:Mice; D009389:Neovascularization, Pathologic; D010634:Phenobarbital / Q000009:adverse effects; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D051926:Basigin; D002273:Carcinogens; D004052:Diethylnitrosamine; D010634:Phenobarbital; D019408:Platelet Endothelial Cell Adhesion Molecule-1; C067980:CD68 antigen, human; D000097382:CD68 Molecule