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目的 探讨具有不同潜在转移能力的黑色素瘤细胞恶性表型的演进及其侵袭转移的机制。方法 采用细胞培养 ,p5 3蛋白免疫组化染色 ,PCR- SSCP检测 ,流式细胞术(PCM) ,蛋白酶活性分析 (Zymography)及裸鼠体内异种接种实验。结果 人黑色素瘤细胞中存在有 p5 3基因的突变 ,瘤细胞表面 6 7KD L N- R的荧光阳性率和全部细胞的平均荧光强度大小顺序为 WM45 1>WM983A>WM1341B>WM35。金属蛋白酶 (MMPs)的产生情况为 :早期 WM35不产生 MMPs;WM1341B仅产生 72 KDa(MMP- 2 ) ,不产生 92 KDa(MMP- 9) ;进展期 WM983A和远处转移瘤株 WM45 1均产生 72 KDa和 92 KDa。WM983A和 WM45 1也可见在裸鼠体内形成明显的转移瘤。结论 p5 3基因突变 ,MMPs的产生和细胞表面 6 7KD L N- R的高表达是人黑色素瘤细胞侵袭转移能力获得的关键因素
Objective To investigate the evolution of malignant phenotypes of melanoma cells with different potential metastatic potentials and the mechanism of invasion and metastasis. Methods Cell culture, p53 protein immunohistochemical staining, PCR-SSCP detection, flow cytometry (PCM), protease activity analysis (Zymography) and xenogeneic inoculation in nude mice were used. RESULTS: There was a mutation in the p53 gene in human melanoma cells. The fluorescence positive rate of NK-LN-R on the surface of tumor cells and the average fluorescence intensity of all cells were in the order of WM45 1>WM983A>WM1341B>WM35. The production of metalloproteinases (MMPs) was as follows: early WM35 did not produce MMPs; WM1341B only produced 72 KDa (MMP-2) and did not produce 92 KDa (MMP-9); advanced stage WM983A and distant metastasis strain WM45 1 were all produced. 72 KDa and 92 KDa. WM983A and WM45 1 also showed significant metastasis in nude mice. Conclusion The p53 gene mutation, the production of MMPs and the high expression of 67KD L N-R on the cell surface are the key factors for the invasion and metastasis of human melanoma cells.