Publications (2)10.12 Total impact
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Article: The expression of functional chemokine receptor CXCR4 is associated with the metastatic potential of human nasopharyngeal carcinoma.
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ABSTRACT: Chemokine receptors are implicated in metastasis of several malignant tumors. This study was done to evaluate the contribution of chemokine receptors CXCR4 and CCR7 to metastasis of human nasopharyngeal carcinoma. Reverse transcription-PCR, immunohistochemistry, and flow cytometry were used to evaluate mRNA and protein expression of CXCR4 and CCR7 in nasopharyngeal carcinoma tumor tissues and cell lines. Chemotaxis assays were used to evaluate the function of CXCR4 in nasopharyngeal carcinoma cells. Antisense CXCR4 was used to inhibit receptor expression and to block metastasis of human nasopharyngeal carcinoma cells in vivo in athymic mice. CXCR4 protein was detected in tumor cells in 31 of 40 primary human nasopharyngeal carcinoma and in 13 of 15 lymph node metastases. CXCR4 transcripts were detected in eight CXCR4 protein-positive primary nasopharyngeal carcinoma tissues and seven nasopharyngeal carcinoma cell lines tested. On the other hand, the transcripts for CCR7 were detected only in four primary nasopharyngeal carcinoma tissues and in none of the nasopharyngeal carcinoma cell lines. In functional experiments, metastatic nasopharyngeal carcinoma cell lines that expressed high levels of CXCR4 were found to migrate in response to the CXCR4 ligand SDF-1alpha. Transfection of antisense CXCR4 in metastatic nasopharyngeal carcinoma cells inhibited the expression of CXCR4 and SDF-1alpha-induced cell migration in vitro and reduced the capacity of the tumor cells to form metastasis in the lungs and lymph nodes when injected in athymic mice. The expression of functional CXCR4 but not CCR7 is correlated with the metastatic potential of human nasopharyngeal carcinoma cells. Therefore, CXCR4 may be considered as a potential target for the prevention of nasopharyngeal carcinoma metastasis.Clinical Cancer Research 08/2005; 11(13):4658-65. · 7.74 Impact Factor -
Article: Transduction of the gene coding for a human G-protein coupled receptor FPRL1 in mouse tumor cells increases host anti-tumor immunity.
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ABSTRACT: Low antigenicity or development of tolerance is believed to be a major contributor to the escape of malignant tumors from immune surveillance of the host. However, anti-tumor responses can be elicited by concomitant immunization of poorly antigenic tumor cells with homologous xenogeneic proteins as 'altered self' proteins. In our study, anti-tumor, but not anti-xenogeneic antigen, immune responses were generated after transduction of the gene coding for a G-protein coupled human formyl peptide receptor like-1 (FPRL1) into a mouse C26 colon cancer cell line. C26 cells transfected with FPRL1 gene exhibited markedly reduced tumorigenicity in syngeneic mice, in association with the appearance of high levels of antibody activity reacting with both FPRL1 containing and wild type C26 cells. The anti-tumor responses required the participation of CD4+ T lymphocytes, since no tumor rejection was observed in nude mice or in syngeneic mice depleted of CD4+ T cells. Furthermore, mice primed with FPRL1 transfected C26 cells were resistant to subsequent challenge by wild type C26 cells. These results indicate that the presence of human FPRL1 is capable of triggering specific anti-tumor host immune responses against poorly antigenic mouse tumor cells.International Immunopharmacology 07/2005; 5(6):971-80. · 2.38 Impact Factor
