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Deprecated: Implicit conversion from float 300.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cancer+Biol+Ther 2016 ; 17 (5): 558-65 Nephropedia Template TP
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Overexpression of hepatocyte nuclear factor 4? in human mesenchymal stem cells suppresses hepatocellular carcinoma development through Wnt/?-catenin signaling pathway downregulation #MMPMID27124543
Wu N; Zhang YL; Wang HT; Li DW; Dai HJ; Zhang QQ; Zhang J; Ma Y; Xia Q; Bian JM; Hang HL
Cancer Biol Ther 2016[May]; 17 (5): 558-65 PMID27124543show ga
Mesenchymal stem cells (MSCs) hold promise as cellular vehicles for the delivery of therapeutic gene products because they can be isolated, expanded, and genetically modified in vitro and possess tumor-oriented homing capacity in vivo.1 Hepatocyte nuclear factor 4? (HNF4?) is a dominant transcriptional regulator of hepatocyte differentiation and hepatocellular carcinogenesis (HCC).2,3 We have previously demonstrated that overexpression of HNF4? activates various hepatic-specific genes and enhances MSC differentiation.4 However, the extent that overexpression of HNF4? in MSCs influences HCC progression has yet to be examined. Here we sought to investigate what effect MSCs overexpressing HNF4? (MSC-HNF4?) have on human hepatoma cells in vitro and in vivo. Conditioned medium collected from in vitro MSC-HNF4? cultures significantly inhibited hepatoma cell growth and metastasis compared with controls. Additionally, nude mice administered MSC-HNF4? exhibited significantly smaller tumors compared with controls in vivo. Immunoblot analysis of HCC cells treated with MSC-HNF4? displayed downregulated ?-catenin, cyclinD1, c-Myc, MMP2 and MMP9. Taken together, our results demonstrate that MSC-HNF4? inhibits HCC progression by reducing hepatoma cell growth and metastasis through downregulation of the Wnt/?-catenin signaling pathway.