| Summary: | 碩士 === 長庚大學 === 生物醫學研究所 === 97 === The Nasopharyngeal carcinoma (NPC) express the Epstein-Barr virus (EBV)-encoded latent membrane protein-1 (NLMP1) oncogene. The expression of EBV-LMP1 in NPC early stage is considered to be an important role during tumorigenesis. To find out carcinogenic course of N-LMP1, we used a NLMP1-expressing tumor model established by implantation of 3T3/NLMP1 tumor was in BALB/c mice. The study previously observed that new blood vessel in hepatocellular carcinoma would secret CCL3 to promote angiogenesis by autocrine. In addition, in many clinical tumor patients and animal models, also found that a large number of CCL3 in the tumor tissue, once the lack of CCL3 will cause slow tumor growth, so CCL3 for tumor growth plays a important role. We have found there are two major groups of CCL3-producing cells, one group is the CD45+ tumor-infiltrating leukocyte; another group is CD45-cells, we defined as tumor cells. We have further to Gr1 and CD11b to distinguish CD45+ CCL3+ cells and found that most of the CD11bhi cells and Gr1+ CD11b + cells will be secreted CCL3, and the two groups will express the receptor of CCL3 (CCR1). On the other hand, the results of the ELISA indicates that only a tumor cells (E2 cells) under the existing circumstances, the tumor cells do not secrete CCL3, but the tumor single cells (TSC) detect a large number of CCL3 secretion. The result showed that the tumor in tumor micro-environment will express CCL3, and we have found that tumor cells secrete CCL3 showed a high degree of activation and division. Finally, we found that N-LMP1 tumor cells CD11bhi and Gr1 + CD11b + cells express CCL3 that may be related to the tumor angiogenesis. The finding may be important in the future strategic design in the immunotherapy of NPC.
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