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目的探讨GHGKHKNK八肽对小鼠黑色素瘤B16-F10细胞克隆形成与体外侵袭能力的作用及其机制。方法用不同实验方法观察GHGKHKNK八肽对克隆形成能力、细胞侵袭能力及GHGKHKNK八肽对层黏连蛋白受体(LN-R),细胞黏附分子-1(ICAM-1),内皮组织钙黏连素(E-cadherin)在小鼠黑色素瘤B16-F10细胞中表达情况。结果不同剂量GHGKHKNK八肽对小鼠黑色素瘤细胞B16-F10的克隆形成侵袭均有抑制作用,与对照组相比较均有显著性差异;小鼠黑色素瘤细胞B16-F10经免疫细胞化学染色后,可见小鼠黑色素瘤细胞B16-F10LN-R、ICAM-1、E-cadhe-sin表达降低。结论GHGKHKNK八肽可以明显抑制肿瘤细胞的克隆形成、黏附和侵袭能力。
Objective To investigate the effect of GHGKHKNK octapeptide on the formation of murine melanoma B16-F10 cells in vitro and its mechanism of invasion. Methods Different experimental methods were used to observe the effect of GHGKHKNK octapeptide on the formation of colony formation, cell invasion and the effect of GHGKHKNK octapeptide on laminin receptor (LN-R), ICAM-1, E-cadherin expression in mouse melanoma B16-F10 cells. Results The different doses of GHGKHKNK octapeptide inhibited the invasion and development of mouse melanoma B16-F10 cells, which were significantly different from those of the control group. After immunocytochemistry staining of B16-F10 in mouse melanoma cells, The expression of B16-F10LN-R, ICAM-1, E-cadhe-sin in mouse melanoma cells was decreased. Conclusion GHGKHKNK octapeptide can significantly inhibit the clonal formation, adhesion and invasion ability of tumor cells.