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Yuliang Ran

Publications and source records attributed to Yuliang Ran.

4 recordsLinked to original sources

Identification of derlin-1 as a novel growth factor-responsive endothelial antigen by suppression subtractive hybridization.

Endothelial cells play an important regulatory role in embryonic development, reproductive functions, tumor growth and progression. In the present study, the suppression subtractive hybridization (SSH) method was employed to identify differentially expressed genes between non-stimulated endothelial cells and activated endothelial cells. Following mRNA isolation of non-stimulated and hepatocellular carcinoma homogenate-stimulated cells, cDNAs of both populations were prepared and subtracted by suppressive PCR. Sequencing of the enriched cDNAs identified a couple of genes differentially expressed, including derlin-1. Derlin-1 was significantly up-regulated by tumor homogenates, VEGF, and endothelial growth supplements in a dose-dependent manner. Knock-down of derlin-1 triggered endothelial cell apoptosis, inhibited endothelial cell proliferation, and blocked the formation of a network of tubular-like structures. Our data reveal that derlin-1 is a novel growth factor-responsive endothelial antigen that promotes endothelial cell survival and growth.

Antigens, Neoplasm↗

Expression vectors for human-mouse chimeric antibodies.

The production of recombinant antibodies has been generally recognized as time-consuming and labor-intensive. The aim of our study is to construct mammalian expression vectors containing the cDNA encoding the human constant regions and murine variable regions to massively and cost-effectively produce full-length chimeric antibodies. Unique restriction sites flanking the Ig variable region were designed to allow for the replacement of variable regions generated by PCR. Western blot analysis of the chimeric antibodies revealed that the expressed products were of the predicted size, structure and specificity. The usefulness of the vectors was confirmed by construction of human-mouse chimeric antibody-HCAb which secretes murine antibody against the human colorectal cancer. Selected in medium containing gradually increasing methotrexate (MTX), clones with increased expression of the product gene can be efficiently generated. The secretion of recombinant chimeric antibody-HCAb yielded 30 pg cell(-1) day(-1) at 10(-6 )M MTX. With this high-level expression from pools, the convenient and rapid production of over 100 milligram amounts per liter of recombinant antibodies may be achieved, which indicates the significant roles of pYR-GCEVH and pYR-GCEVL in the production of chimeric antibodies.

Animals↗

[Expression and hypoxic regulation of vascular endothelial growth factor and matrix metalloproteinase-9 in esophageal carcinoma].

OBJECTIVE: To investigate the the expression and hypoxic regulation of vascular endothelial growth factor(VEGF) and matrix metalloproteinase-9. METHODS: VEGF mRNA and MMP-9 mRNA were examined by reverse transcription-polymerase chain reaction (RT-PCR) in 43 esophageal carcinoma specimens including 18 para-tumorous esophageal tissues. The expression of VEGF protein and mean microvessel density (MVD) in 56 specimens were examined by immunohistochemical stain. The effect of hypoxia on VEGF and MMP-9 expression in esophageal cancer cell lines was quantitatively determined by enzyme linked immunosorbent assay (ELISA). RESULTS: The VEGF expression in the tumorous tissue, being significantly correlated with MVD in the tumor, was remarkably higher than that in the para-tumorous tissue. VEGF and MVD expression in the tumor was significantly associated with stage and metastasis of esophageal carcinoma. The MMP-9 expression in the tumorous tissue, being uncorrelated with vessel count and clinicopathologic features in esophageal carcinoma, was significantly higher than that in the para-tumorous tissue. Hypoxia significantly increased the VEGF expression in esophageal cancer cell lines but did not affect the MMP-9 expression. CONCLUSIONS: The expression of VEGF plays an important role in the angiogenesis and metastasis of esophageal cancer, which is regulated by hypoxia. VEGF may serve as a predictor of progression in esophageal carcinoma and a potential target for antiangiogenic therapy of esophageal carcinoma.

Endothelial Growth Factors↗

Monoclonal antibody to human esophageal cancer endothelium inhibits angiogenesis and tumor growth.

BACKGROUND: Monoclonal antibodies to tumor endothelial cells (TECs) hold great promise for cancer angiogenesis-targeted therapy. The aim of the present study was to develop such an agent for esophageal cancer treatment. MATERIALS AND METHODS: BALB/c mice were immunized with human esophageal tumor endothelial cells (ETECs) cultured with tumor homogenate. MAbs were produced, screened by immunofluorescence and immunohistochemistry (IHC) and an IgG1K mAb 4B3 was selected. The mAb 4B3 antigen was analyzed by IHC and Western blotting. The antibody's effects on ETECs were determined by adhesion and tube formation assays, while its therapeutic potential was evaluated with a tumor model established by co-inoculating mice with the human esophageal cancer cell lines KYSE180 and ETECs. RESULTS: MAb 4B3 recognized a 40-kDa surface antigen preferentially expressed on TECs and other stromal cells in human malignant tissues of esophagus, stomach, colon, liver, lung and breast compared with their normal counterparts. The antigen was not detected on cancer cells or normal epithelia in these tissues, nor was it detectable on any cells in the mouse xenografts of KYSE180, including the host endothelia. MAb 4B3 inhibited ETEC adhesion to extracellular matrix proteins and tube formation in vitro. The antibody inhibited angiogenesis and growth of the tumor formed by coinoculation. CONCLUSION: These results suggest that mAb 4B3 has therapeutic potential for esophageal cancer.

Animals↗