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Targeting SHCBP1 Inhibits Cell Proliferation in Human Hepatocellular Carcinoma Cells
Tao, Han-Chuan,Wang, Hai-Xiao,Dai, Min,Gu, Cheng-Yu,Wang, Qun,Han, Ze-Guang,Cai, Bing Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.10
Src homology 2 domain containing (SHC) is a proto-oncogene which mediates cell proliferation and carcinogenesis in human carcinomas. Here, the SHC SH2-domain binding protein 1 (SHCBP1) was first established to be up-regulated in human hepatocellular carcinoma (HCC) tissues by array-base comparative genome hybridization (aCGH). Meanwhile, we examine and verify it by quantitative real-time PCR and western blot. Our current data show that SHCBP1 was up-regulated in HCC tissues. Overexpression of SHCBP1 could significantly promote HCC cell proliferation, survival and colony formation in HCC cell lines. Furthermore, knockdown of SHCBP1 induced cell cycle delay and suppressed cell proliferation. Furthermore, SHCBP1 could regulate the expression of activate extracellular signal-regulated kinase 1/2 (ERK1/2) and cyclin D1. Together, our findings indicate that SHCBP1 may contribute to human hepatocellular carcinoma by promoting cell proliferation and may serve as a molecular target of cancer therapy.
( Xiao Dong Li ),( Myong Jong YI ),( Yow Han Son ),( Guang Ze Jin ),( Kyeong Hak Lee ),( Yeong Mo Son ),( Rae Hyun Kim ) 한국임학회 2010 한국산림과학회지 Vol.99 No.5
Publications with the data on allometric equation, biomass and productivity of major oak forests in Korea were reviewed. Different allometric equations of major oak species showed site- or species-specific dependences. The biomass of major oak forests varied with age, dominant species, and location. Aboveground tree biomass over the different oak species was expressed as a power equation of the stand age. The proportion of tree component (tem, branch and leaf) to total aboveground biomass differed among oak species, however, biomass ranked stem>branch>leaf in general. The leaf biomass allocation over the different oak species was expressed as a power equation of total aboveground biomass while there were no significant patterns of biomass allocation from stem and branch to the aboveground biomass. Tree root biomass continuously increased with the aboveground biomass for the major oak forests. The relationship between the root to shoot ratio and the aboveground tree biomass was expressed by a logarithmic equation for major oak forests in Korea. Thirteen sets of data were used for estimating the net primary production (NPP) and net ecosystem production (NEP) of oak forests. The mean PP and NEP across different oak forests was 10.2 and 1.9 Mg C ha-1 year-1. The results in biomass allocation, NPP and NEP generally make Korean oak forests an important carbon sinks.
Ectopic Overexpression of COTE1 Promotes Cellular Invasion of Hepatocellular Carcinoma
Zhang, Hai,Huang, Chang-Jun,Tian, Yuan,Wang, Yu-Ping,Han, Ze-Guang,Li, Xiang-Cheng Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.11
Family with sequence similarity 189, member B (FAM189B), alias COTE1, a putative oncogene selected by microarray, for the first time was here found to be significantly up-regulated in hepatocellular carcinoma (HCC) specimens and HCC cell lines. mRNA expression of COTE1 in HCC samples and cell lines was detected by reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR, while protein expression of COTE1 in HCC tissues was assessed by immunohistochemistry. In addition, invasion of HCC cells was observed after overexpressing or silencing COTE1. In the total of 48 paired HCC specimens, compared with the adjacent non-cancer tissues, the expression of COTE1 was up-regulated in 31 (p<0.01). In HCC cell lines, COTE1 expression was significantly higher than in normal human adult liver (p<0.01). Overexpression of COTE1 enhanced HCC-derived LM6 and MHCC-L cellular invasion in vitro. In contrast, COTE1 knockdown via RNAi markedly suppressed these phenotypes, as documented in LM3 and MHCC-H HCC cells. Mechanistic analyses indicated that COTE1 could physically associate with WW domain oxidoreductase (WWOX), a tumor suppressor. COTE1 may be closely correlated with invasion of hepatocellular carcinoma (HCC) cells and thus may serve as an effective target for gene therapy.
Up-regulation of NICE-3 as a Novel EDC Gene Could Contribute to Human Hepatocellular Carcinoma
Wei, Yuan-Jiang,Hu, Qin-Qin,Gu, Cheng-Yu,Wang, Yu-Ping,Han, Ze-Guang,Cai, Bing Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.9
The epidermal differentiation complex (EDC) contains a large number of gene products which are crucial for the maturation of the human epidermis and can contribute to skin diseases, even carcinogenesis. It is generally accepted that activation of oncogenes and/or inactivation of tumor suppressor genes play pivotal roles in the process of carcinogenesis. Here, NICE-3, a novel EDC gene, was found to be up-regulated in human hepatocellular carcinoma (HCC) by quantitative real-time RT-PCR. Furthermore, overexpression of exogenous NICE-3 by recombinant plasmids could significantly promote cell proliferation, colony formation and soft agar colony formation in Focus and WRL-68 HCC cell lines. Reversely, NICE-3 silencing by RNA interference could markedly inhibit these malignant phenotypes in YY-8103 and MHCC-97H cells. Moreover, cell cycle analysis of MHCC-97H transfected with siRNA by flow cytometry showed that NICE-3 knockdown may inhibit cell growth via arrest in G0/G1 phase and hindering entry of cells into S phase. All data of our findings indicate that NICE-3 may contribute to human hepatocellular carcinoma by promoting cell proliferation.
( Hai Xiao Wang ),( Kuang Jie Wu ),( Yuan Sun ),( Yan Dong Li ),( Ming Yu Wu ),( Qian Qiao ),( Yuan Jiang Wei ),( Ze Guang Han ),( Bing Cai ) 생화학분자생물학회(구 한국생화학분자생물학회) 2012 BMB Reports Vol.45 No.11
The human glycoprotein, stanniocalcin 2 (STC2) plays multiple roles in several tumor types, however, its function and clinical significance in hepatocellular carcinoma (HCC) remain unclear. In this study, we detected STC2 expression by quantitative real-time PCR and found STC2 was upregulated in HCC tissues, correla ed with tumor size and multiplicity of HCC. Ectopic expression of STC2 markedly promoted HCC cell proliferation and colony formation, while silencing of endogenous STC2 resulted in a reduced cell growth by cell cycle delay in G0/G1 phase. Western blot analysis demonstrated that STC2 could regulate the expression of cyclin D1 and activate extracellular signal-regulated kinase 1/2 (ERK1/2) in a dominant-positive manner. Transwell chamber assay also indicated altered patterns of STC2 expression had an important effect on cell migration. Our findings suggest that STC2 functions as a potential oncoprotein in the development and progression of HCC as well as a promising molecular target for HCC therapy.
( Di Wu ),( Hong Wu Wang ),( Tao Chen ),( Yong Zou ),( Wei Ming Yan ),( Mei Fang Han ),( Ze Guang Wu ),( Xiao Jing Wang ) 대한간학회 2013 춘·추계 학술대회 (KASL) Vol.2013 No.1
Aims: The underlying pathogenesis of fulminant viral hepatitis (FVH) has not been fully elucidated. As a subset of regulatory T cells, CD3+CD4-CD8- double negative (DN) T cells can suppress T cell responses. In this study, we present new insights into the immune mediated mechanisms involved in FVH caused by murine hepatitis virus strain 3 (MHV-3). Methods: The phenotype and cytokines of DN T cells were detected by flow cytometric analysis. The levels of mfgl2 were measured by real-time PCR and western-blot. The function of mfgl2 was measured by PCA. Results: After MHV-3 infection, the proportions of DN T cells increased significantly in BALB/cJ mice, and splenic DN T cells expressing high levels of CD69 were recruited by MHV-3 infected hepatocytes to the liver. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBil) increased, accompanied by massive hepatocyte necrosis. These DN T cells were predominantly consisted of a TCRαβ+ subset expressing high levels of CD44, and did not produce cytokine except IL-2. Adoptive transfer of this subset of DN T cells to the MHV-3 infected mice resulted in an increase of murine fibrinogen-like protein 2 (mfgl2) expression in association with massive fibrin deposition in the liver. Following MHV-3 infection, membrane mfgl2 expression and functional procoagulant activity (PCA) increased remarkably in the DN T cells. Introduction of a recombinant adenovirus which encoded a microRNA specifically targeting mfgl2 gene (Ad-mfgl2-miRNA) in vivo significantly inhibited the hepatic expression of mfgl2, increased mice survival. However, under this condition, adoptive transfer of the DN T cells accelerated the disease progression and reversed the benefit from mfgl2 gene silence, led to a 100% death. Conclutions: Our results demonstrated that DN T cell-derived mfgl2 may serve as an important effector molecule contributing to the pathogenesis of MHV-3-induced FVH.