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Articles by J Fu
Total Records ( 8 ) for J Fu
  C Zhang , L Fu , J Fu , L Hu , H Yang , T. H Rong , Y Li , H Liu , S. B Fu , Y. X Zeng and X. Y. Guan
 

Purpose: Tumor fibroblasts (TF) have been suggested to play an essential role in the complex process of tumor-stroma interactions and tumorigenesis. The aim of the present study was to investigate the specific role of TF in the esophageal cancer microenvironment.

Experimental Design: An Affymetrix expression microarray was used to compare gene expression profiles between six pairs of TFs and normal fibroblasts from esophageal squamous cell carcinoma (ESCC). Differentially expressed genes were identified, and a subset was evaluated by quantitative real-time PCR and immunohistochemistry.

Results: About 43% (126 of 292) of known deregulated genes in TFs were associated with cell proliferation, extracellular matrix remodeling, and immune response. Up-regulation of fibroblast growth factor receptor 2 (FGFR2), which showed the most significant change, was detected in all six tested TFs compared with their paired normal fibroblasts. A further study found that FGFR2-positive fibroblasts were only observed inside the tumor tissues and not in tumor-surrounding stromal tissues, suggesting that FGFR2 could be used as a TF-specific marker in ESCC. Moreover, the conditioned medium from TFs was found to be able to promote ESCC tumor cell growth, migration, and invasion in vitro.

Conclusions: Our study provides new candidate genes for the esophageal cancer microenvironment. Based on our results, we hypothesize that FGFR2(+)-TFs might provide cancer cells with a suitable microenvironment via secretion of proteins that could promote cancer development and progression through stimulation of cancer cell proliferation, induction of angiogenesis, inhibition of cell adhesion, enhancement of cell mobility, and promotion of the epithelial-mesenchymal transition.

  K Anastassiadis , J Fu , C Patsch , S Hu , S Weidlich , K Duerschke , F Buchholz , F Edenhofer and A. F. Stewart
  Konstantinos Anastassiadis, Jun Fu, Christoph Patsch, Shengbiao Hu, Stefanie Weidlich, Kristin Duerschke, Frank Buchholz, Frank Edenhofer, and A. Francis Stewart

Tyrosine site-specific recombinases (SSRs) including Cre and FLP are essential tools for DNA and genome engineering. Cre has long been recognized as the best SSR for genome engineering, particularly in mice. Obtaining another SSR that is as good as Cre will be a valuable addition to the genomic toolbox. To this end, we have developed and validated reagents for the Dre-rox system. These include an Escherichia coli-inducible expression vector based on the temperature-sensitive pSC101 plasmid, a mammalian expression vector based on the CAGGs promoter, a rox-lacZ reporter embryonic stem (ES) cell line based on targeting at the Rosa26 locus, the accompanying Rosa26-rox reporter mouse line, and a CAGGs-Dre deleter mouse line. We also show that a Dre-progesterone receptor shows good ligand-responsive induction properties. Furthermore, we show that there is no crossover recombination between Cre-rox or Dre-loxP. Hence, we add another set of efficient tools to the genomic toolbox, which will enable the development of more sophisticated mouse models for the analysis of gene function and disease.

  S Ju , Y Ge , H Qiu , B Lu , Y Qiu , J Fu , G Liu , Q Wang , Y Hu , Y Shu and X. Zhang
 

Dendritic cells (DCs) are responsible for the initiation of immune responses. Our study demonstrates a new pathway for generating a large quantity of stimulatory monocyte-derived DCs (Mo-DCs) from human monocytes using anti-4-1BB ligand (4-1BBL) mAb to trigger reverse signaling. The anti-4-1BBL-driven Mo-DCs (DCs-4-1BBL) not only express higher levels of CD86, CD83 and HLA-DR, when compared with the Mo-DCs matured by tumor necrosis factor , but also exhibit a unique phenotype that expresses lower levels of PD-L1. High levels of GM-CSF, M-CSF and Flt3 ligand (FL) were found in the anti-4-1BBL-differentiation culture. Neutralizing M-CSF, GM-CSF and FL inhibited Mo-DC proliferation stimulated by anti-4-1BBL mAb, suggesting that M-CSF, GM-CSF and FL are involved in cell proliferation stimulated by anti-4-1BBL. Further analysis of the DCs-4-1BBL showed increased secretion of Th1-type cytokines IL-12 and IFN- and decreased secretion of IL-10. DCs-4-1BBL induced much stronger proliferative responses in the mixed lymphocyte reaction assay when compared with DCs derived by GM-CSF. Moreover, DCs-4-1BBL preferentially induced Th1 responses. We have further demonstrated that anti-4-1BBL antibody stimulated nuclear translocation of NF-B from the cytoplasm in monocytes, suggesting that reverse signaling by 4-1BBL is likely responsible for mediating DC differentiation. Collectively, we have found that reverse signaling of 4-1BBL promotes the differentiation of potent Th1-inducing DCs from human monocytes.

  C Liu , G Tian , Y Tu , J Fu , C Lan and N. Wu
  Objective

Bone morphogenetic protein-2 (BMP-2) is normally expressed in the embryo promoting the development of several organs. Aberrant expression of BMP-2 occurs in various tumors. However, a correlation between BMP-2 expression in human gliomas and patients' prognosis has not been reported. To address this question, this study was to investigate the BMP-2 expression pattern in human gliomas and to evaluate its prognostic relevance.

Methods

We analyzed the expression of the BMP-2 antigen in a series of 98 gliomas of various grade and histology by immunohistochemistry on paraffin-embedded sections. Then, the correlation of BMP-2 expression pattern with clinical–pathological features of patients and its prognostic relevance were determined.

Results

Immunohistochemical analysis with anti-BMP-2 antibody revealed dense and spotty staining in the tumor cells and its expression levels became significantly higher as the gliomas' grade advanced (P < 0.001). The median survival of patients with intensively positive BMP-2 expression was significantly shorter than that with negative expression (318 vs. 1197 days, P < 0.0001). The Kaplan–Meier survival curves showed that the BMP-2 expression was not only a significant predictor of survival in high-grade gliomas (grade IV, P = 0.02), but also in lower-grade gliomas (grades II and III, P < 0.001).

Conclusions

These results indicate that BMP-2 is a highly sensitive marker for gliomas prognosis and suggest that the expression level of BMP-2 may be a potent tool for the clinical prognosis of gliomas patients.

  Y Tu , J Lu , J Fu , Y Cao , G Fu , R Kang , X Tian and B. Wang
  Objective

Neuroepithelial-transforming protein 1 is a member of the guanine nucleotide exchange factor family, a group of proteins which are known to activate and thereby regulate Rho family members. Deregulation of neuroepithelial-transforming protein 1 expression has been found in certain types of human tumors. To investigate its prognostic value in human gliomas, which is currently unknown, we examined the correlation between neuroepithelial-transforming protein 1 expression and prognosis in patients with gliomas.

Methods

Immunohistochemical staining was performed to detect neuroepithelial-transforming protein 1 expression patterns in the biopsies from 96 patients with primary gliomas. Kaplan–Meier survival and Cox's regression analyses were performed to evaluate the prognosis of patients.

Results

Immunohistochemical analysis with anti-neuroepithelial-transforming protein 1 antibody revealed that neuroepithelial-transforming protein 1 was significantly associated with the Karnofsky performance scale score and World Health Organization grades of patients with gliomas. Especially, the positive expression rates of neuroepithelial-transforming protein 1 were significantly higher in patients with higher grade (P = 0.001) and lower Karnofsky's performance scale score (P = 0.005). The median survival of patients with high neuroepithelial-transforming protein 1 expression was significantly shorter than that with low expression and without expression (316, 892 and 1180 days, respectively). Cox's multifactor analysis showed that the Karnofsky performance scale (P = 0.01), World Health Organization grade (P = 0.008) and neuroepithelial-transforming protein 1 (P = 0.006) were independent prognosis factors for human glioma.

Conclusions

Taken together, our study indicates for the first time that neuroepithelial-transforming protein 1 status may be a highly sensitive marker for glioma prognosis and suggest that the expression patterns of neuroepithelial-transforming protein 1 might be a potent tool for predicting the clinical prognosis of glioma patients.

  J Fu , X Chen , Y Zhang , H Gu and Y. Bai
  Objective

To investigate the possible role of CD147 and vascular endothelial growth factor in progression and prognosis of acute myeloid leukemia.

Methods

Immunohistochemical staining was performed to detect the expression of CD147 and vascular endothelial growth factor in paraffin-embedded sections from 62 bone marrow biopsies obtained from an equal number of patients with newly diagnosed acute myeloid leukemia.

Results

CD147 and vascular endothelial growth factor expression in the bone marrow of acute myeloid leukemia patients were significantly higher than those in normal controls (both P < 0.001). Expression of them was significantly increased in patients with a high degree of microvessel density compared with those with a low degree (CD147: P = 0.009; vascular endothelial growth factor: P = 0.01) and correlated well with bone marrow microvessel density (CD147: P = 0.01; vascular endothelial growth factor: P = 0.02). In addition, higher levels of CD147 and vascular endothelial growth factor were also found in acute myeloid leukemia patients with an unfavorable karyotype compared with those with intermediate and favorable karyotypes (both P = 0.01). Moreover, the expression of CD147 was significantly correlated with that of vascular endothelial growth factor (P < 0.001). Furthermore, the co-expression of CD147 and vascular endothelial growth factor in the bone marrow indicated a poor prognosis in acute myeloid leukemia and was an independent prognostic factor for overall survival by multivariate analysis.

Conclusions

Our data show for the first time that the co-expression of CD147 and vascular endothelial growth factor may indicate a poor prognosis in acute myeloid leukemia and may be a highly sensitive marker for predicting the clinical outcome of patients.

  P Jiang , S. N Rushing , C. w Kong , J Fu , D. K. T Lieu , C. W Chan , W Deng and R. A. Li
 

Human embryonic stem cells (hESCs) can self-renew while maintaining their pluripotency. Direct reprogramming of adult somatic cells to induced pluripotent stem cells (iPSCs) has been reported. Although hESCs and human iPSCs have been shown to share a number of similarities, such basic properties as the electrophysiology of iPSCs have not been explored. Previously, we reported that several specialized ion channels are functionally expressed in hESCs. Using transcriptomic analyses as a guide, we observed tetraethylammonium (TEA)-sensitive (IC50 = 3.3 ± 2.7 mM) delayed rectifier K+ currents (IKDR) in 105 of 110 single iPSCs (15.4 ± 0.9 pF). IKDR in iPSCs displayed a current density of 7.6 ± 3.8 pA/pF at +40 mV. The voltage for 50% activation (V1/2) was –7.9 ± 2.0 mV, slope factor k = 9.1 ± 1.5. However, Ca2+-activated K+ current (IKCa), hyperpolarization-activated pacemaker current (If), and voltage-gated sodium channel (NaV) and voltage-gated calcium channel (CaV) currents could not be measured. TEA inhibited iPSC proliferation (EC50 = 7.8 ± 1.2 mM) and viability (EC50 = 5.5 ± 1.0 mM). By contrast, 4-aminopyridine (4-AP) inhibited viability (EC50 = 4.5 ± 0.5 mM) but had less effect on proliferation (EC50 = 0.9 ± 0.5 mM). Cell cycle analysis further revealed that K+ channel blockers inhibited proliferation primarily by arresting the mitotic phase. TEA and 4-AP had no effect on iPSC differentiation as gauged by ability to form embryoid bodies and expression of germ layer markers after induction of differentiation. Neither iberiotoxin nor apamin had any function effects, consistent with the lack of IKCa in iPSCs. Our results reveal further differences and similarities between human iPSCs and hESCs. A better understanding of the basic biology of iPSCs may facilitate their ultimate clinical application.

 
 
 
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