| Summary: | 碩士 === 國立臺灣大學 === 基因體暨蛋白體醫學研究所 === 105 === Tumor-neovascularization is a physiological process in cancer progression, which contributes in controlling tumor growth and cancer metastasis. Recently, scientists found that except angiogenesis, cancer cell could form tubule-like structure by itself called vascular mimicry (VM), which is one of the major types of tumor-neovascularization. Until now, the molecular mechanism of VM remains unclear; but some literatures indicated that this phenomenum may relate to the process of epithelial-mesenchymal transition (EMT) and cancer stemness. In the past, we identified that Long Form Collapsin Response Mediator Protein-1 (LCRMP-1), an isoform of CRMP-1, is a metastasis enhancer and its expression was positively correlated with poor clinical outcome in non-small cell lung cancer (NSCLC). Recently, we found that the expressions of LCRMP-1 were positively correlated with the blood vessel density in lung cancer tissues; in addition, LCRMP-1 stable cells could form tube structures on matrigel by theirselves. The above findings let us hypothesize whether LCRMP-1 is involved in tumor vascular mimicry. In this study, we tried to explore the role of LCRMP-1 participated in VM through several cellular and molecular assays. Our data showed that overexpression of LCRMP-1 could let CL1-0 cells form tubular structures on Matrigel with a dose-dependent manner; whereas silencing the expression of LCRMP-1 in CL1-5 had the counter effect. Moreover, we found that the LCRMP-1 induced VM might through regulation of mesenchymal-endothelial like transition but less correlated with cancer stemness. Although this is a phenomenon study, the identification of the potential role of LCRMP-1 in VM may provide hints for further exploring the detail mechanism in the near future.
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