Lentivirus-Based DsRed-2-Transfected Pancreatic Cancer Cells for Deep In Vivo Imaging of Metastatic Disease

Zhou, Jiahua; Yu, Zhenxin; Zhao, Susu; Hu, Liang; Zheng, Jie; Yang, Di; Bouvet, Michael; Hoffman, Robert M.

doi:10.1016/j.jss.2008.08.027

Cited by 14 publications

(7 citation statements)

References 20 publications

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“…Orthotopic pancreatic cancer models were established simultaneously in both groups of mice. The detailed procedures for establishing orthotopic pancreatic cancer were described in our previous study [27]. After establishment of the model, the 2 groups of mice were each further randomly divided into 2 subgroups (WT and WT+SB; DM and DM+SB).…”

Section: Methodsmentioning

confidence: 99%

Diabetes mellitus stimulates pancreatic cancer growth and epithelial-mesenchymal transition-mediated metastasis via a p38 MAPK pathway

et al. 2016

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Diabetes mellitus (DM) and its accompanying chronic inflammation promote tumor progression. p38 mitogen-activated protein kinase (MAPK) is an essential kinase for inflammation. The effects of p38 MAPK on epithelial-mesenchymal transition (EMT)-mediated diabetic pancreatic cancer metastasis remain unclear. Here, we demonstrate that p38 MAPK phosphorylation was significantly increased in pancreatic cancer cells treated with high glucose and in pancreatic tumors from diabetic animals. A p38 MAPK inhibitor significantly suppressed the proliferation and invasion of pancreatic cancer cells under high-glucose conditions. Moreover, p38 MAPK inhibition not only significantly decreased both the tumor volume monitored by magnetic resonance imaging and EMT-related metastasis but also increased the survival of diabetic mice bearing pancreatic tumors. Furthermore, the inflammation in diabetic animals bearing pancreatic tumors was also significantly lower after therapy. Collectively, our findings reveal that p38 MAPK inhibitors may provide a novel intervention strategy for diabetic pancreatic cancer treatment.

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Section: Methodsmentioning

confidence: 99%

Diabetes mellitus stimulates pancreatic cancer growth and epithelial-mesenchymal transition-mediated metastasis via a p38 MAPK pathway

et al. 2016

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“…The full length HCV core cDNA was cloned into lentiviral vector, pCSII-EF plasmid, to create the pCSII-EF-HCV core[32]. The pCSII-EF-HCV core or control pCSII-EF-IRES-GFP plasmid was transfected into HEK293T cells together with two packaging plasmids, pCAG-HIVgp and pCMV-VSV-G/RSV-Rev (provided by the RIKEN Bio-resource Center), using the calcium phosphate method.…”

Section: Methodsmentioning

confidence: 99%

HCV Infection Enhances Th17 Commitment, Which Could Affect the Pathogenesis of Autoimmune Diseases

et al. 2014

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BackgroundVarious kinds of autoimmune diseases have been reported to have a significant relationship with persistent hepatitis c virus (HCV) infection and Th17 cells. Previously, our group reported that the existence of HCV in T lymphocytes could affect the development of CD4+ helper T cells and their proliferation, in addition to the induction of immunoglobulin hyper-mutation.MethodsTherefore, we analyzed the relationship between persistent infection of HCV and the mechanism of Th17 cell induction ex vivo and in vitro.ResultsThe prevalence of autoimmune-related diseases in chronic hepatitis c patients (CH-C) was significantly higher than in other types of chronic hepatitis (hepatitis B and NASH). A significantly higher frequency of IL6 and TGF-β double-high patients was detected in CH-C than in other liver diseases. Moreover, these double-high patients had significantly higher positivity of anti-nuclear antibody, cryoglobulinemia, and lymphotropic HCV and higher amounts of IL1-β, IL21, IL23. In addition to the previously reported lymphotropic SB-HCV strain, we found a novel, genotype 1b lymphotropic HCV (Ly-HCV), by deep sequencing analysis. Lymphotropic-HCV replication could be detected in the lymphoid cells with various kinds of cytokine-conditions including IL1β, IL23, IL6 and TGF-β in vitro. Infection by HCV could significantly enhance the development of Th17 cells. The HCV protein responsible for inducing the Th17 cells was HCV-Core protein, which could enhance the STAT-3 signaling and up-regulate the expression of RORγt as a Th17 master gene.ConclusionInfection by lymphotropic HCV might enhance the Th17 development and contribute to understanding the pathogenesis of autoimmune-related diseases.

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“…For EpCAM expression, EpCAM cDNA was inserted into a lentiviral vector, the pCSII‐EF plasmid. ( 34 ) The pCSII‐EF‐EpCAM or control pCSII‐EF‐IRES‐GFP plasmid was transfected into HEK293T cells together with two packaging plasmids, pCAG‐HIVgp and pCMV‐VSV‐G/RSV‐Rev (provided by the RIKEN Bio‐resource Center), using the calcium phosphate method. The supernatants containing the recombinant lentivirus were used for the infection of EpCAM − or EpCAM + cells.…”

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confidence: 99%

Characterization of the epithelial cell adhesion molecule (EpCAM)⁺ cell population in hepatocellular carcinoma cell lines

Kimura

Takahashi²,

Ishii³

et al. 2010

Cancer Science

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Accumulating evidence suggests that cancer stem cells (CSC) play an important role in tumorigenicity. Epithelial cell adhesion molecule (EpCAM) is one of the markers that identifies tumor cells with high tumorigenicity. The expression of EpCAM in liver progenitor cells prompted us to investigate whether CSC could be identified in hepatocellular carcinoma (HCC) cell lines. The sorted EpCAM+ subpopulation from HCC cell lines showed a greater colony formation rate than the sorted EpCAM− subpopulation from the same cell lines, although cell proliferation was comparable between the two subpopulations. The in vivo evaluation of tumorigenicity, using supra‐immunodeficient NOD/scid/γcnull (NOG) mice, revealed that a smaller number of EpCAM+ cells (minimum 100) than EpCAM− cells was necessary for tumor formation. The bifurcated differentiation of EpCAM+ cell clones into both EpCAM+ and EpCAM− cells was obvious both in vitro and in vivo, but EpCAM− clones sustained their phenotype. These clonal analyses suggested that EpCAM+ cells may contain a multipotent cell population. Interestingly, the introduction of exogenous EpCAM into EpCAM+ clones, but not into EpCAM− clones, markedly enhanced their tumor‐forming ability, even though both transfectants expressed a similar level of EpCAM. Therefore, the difference in the tumor‐forming ability between EpCAM+ and EpCAM− cells is probably due to the intrinsic biological differences between them. Collectively, our results suggest that the EpCAM+ population is biologically quite different from the EpCAM− population in HCC cell lines, and preferentially contains a highly tumorigenic cell population with the characteristics of CSC. (Cancer Sci 2010)

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Lentivirus-Based DsRed-2-Transfected Pancreatic Cancer Cells for Deep In Vivo Imaging of Metastatic Disease

Cited by 14 publications

References 20 publications

Diabetes mellitus stimulates pancreatic cancer growth and epithelial-mesenchymal transition-mediated metastasis via a p38 MAPK pathway

Diabetes mellitus stimulates pancreatic cancer growth and epithelial-mesenchymal transition-mediated metastasis via a p38 MAPK pathway

HCV Infection Enhances Th17 Commitment, Which Could Affect the Pathogenesis of Autoimmune Diseases

Characterization of the epithelial cell adhesion molecule (EpCAM)⁺ cell population in hepatocellular carcinoma cell lines

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Lentivirus-Based DsRed-2-Transfected Pancreatic Cancer Cells for Deep In Vivo Imaging of Metastatic Disease

Cited by 14 publications

References 20 publications

Diabetes mellitus stimulates pancreatic cancer growth and epithelial-mesenchymal transition-mediated metastasis via a p38 MAPK pathway

Diabetes mellitus stimulates pancreatic cancer growth and epithelial-mesenchymal transition-mediated metastasis via a p38 MAPK pathway

HCV Infection Enhances Th17 Commitment, Which Could Affect the Pathogenesis of Autoimmune Diseases

Characterization of the epithelial cell adhesion molecule (EpCAM)+ cell population in hepatocellular carcinoma cell lines

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Characterization of the epithelial cell adhesion molecule (EpCAM)⁺ cell population in hepatocellular carcinoma cell lines