黑色素细胞瘤细胞成瘤性的缺失情况及其机制

Tumorigenicity absence and its mechanism of melanocytoma cells

目的探讨黑色素细胞瘤细胞系成瘤能力的缺失情况及其机制。方法选取对数生长期人黑色素细胞瘤细胞系和人A375黑色素瘤细胞系,分别皮下注射至5只裸鼠右侧腋下,4个月后观察是否成瘤。取原代及传代培养的黑色素细胞瘤细胞系和黑色素瘤细胞系进行镜下观察,了解其体外成瘤情况。检测两种细胞系血管内皮生长因子(VEGF)、CD31和CD133 m RNA的表达情况。结果裸鼠皮下异种移植4个月后,黑色素细胞瘤细胞系未能成瘤,而黑色素瘤细胞系成瘤率100%。镜下发现黑色素瘤细胞可见细胞典型克隆,而黑色素细胞瘤细胞仅部分出现克隆样生长方式。黑色素细胞瘤细胞的VEGF和CD31 m RNA的表达水平低于黑色素瘤细胞系(P<0.05)。结论黑色素细胞瘤细胞致瘤性缺失,其血管生成基因表达减弱而导致血管生成能力的低下可能是成瘤性缺失的机制之一。

Objective To explore the absence of tumorigenicity and its mechanism of melanocytoma cells. Methods Human melanocytoma cell line and human A375 melanoma cell line during logarithmic phase were selected,and each cell line was subcutaneously injected into the right axillas of five nude mice. The tumor growth was observed after four months. The melanocytoma cell line and melanoma cell line in primary culture and subculture were selected and were observed under microscope to assess the tumorigenicity in vitro. The expressions of vascular endothelial growth factor（ VEGF）,CD31 and CD133 m RNAs were detected in the two cell lines. Results After four months of subcutaneous xenografting in nude mice,tumor lesion was not found in the melanocytoma cell line,but the tumorigenicity rate was 100% in the melanoma cell line. Microscopic findings showed that classic cell clone was observed in the melanoma cells,but only clone-like growth was found in some melanocytoma cells. The expression levels of VEGF and CD31 in the melanocytoma cells were lower than those in the melanoma cells（ P 0. 05）. Conclusion Tumorigenicity is absent in the melanocytoma cell line,and the reduced ability of angiogenesis due to decreased expressions of angiogenesis-related genes probably is one of its mechanisms.