摘要
目的:探讨白细胞介素-23(IL-23)对黑色素瘤B16F10细胞增殖和侵袭能力的影响。方法:体外培养小鼠黑色素瘤B16F10细胞,采用MTT法检测IL-23对B16细胞增殖能力的影响;Transwell侵袭实验检测IL-23对B16细胞侵袭能力的影响;明胶酶谱法分析IL-23处理后肿瘤细胞B16细胞分泌MMP-2和MMP-9的活性表达情况。免疫印迹杂交法检测IL-23处理组肿瘤细胞核转录因子κB P65(NF-κB P65)的表达水平。结果:与对照组相比,IL-23处理组B16F10细胞穿膜数明显增多(P<0.01);肿瘤细胞MMP-2和MMP-9的表达活性增强(P<0.01);核转录因子NF-κB P65的表达水平显著提高(P<0.01);B16细胞的增殖能力未见明显变化(P>0.05)。结论:IL-23对黑色素瘤B16F10细胞的增殖能力无影响,可通过上调MMP-2和MMP-9的活性促进肿瘤细胞侵袭,其分子机制可能与NF-κB信号通路的激活相关。
Objective: To investigate the effects of interlukin-23 (IL-23) on the proliferation and invasion of mouse B16F10 melanoma cells. Methods: Mouse B16 melanoma cells were cultured in vitro. Cells in research were treated with and without a certain-concentration IL-23 respectively. The proliferation of B16 cells was determined by MTT. And the invasion of B16 cells was detected by Transwell experiment. The expression activities of MMP-2 and MMP-9 were analyzed by Gelatin Zymography and NF-KB phosphorylated P65 expression was measured by Western blot. Results: The growth rate of B16 cells treated with IL-23 did not show significant change (P〉0.05) compared with the control group. Matrigel invasion assay revealed that addition of IL-23 to B16 cells significantly enhanced its invasive properties (P〈0.01), and Gelatin Zymography analysis showed that the MMP-9 activity of B16F10 cells was significantly increased by IL-23 (P〈0.01). IL-23 induced an increased NF-KB phosphorylated P65 expression in B16 cells. Conclusion: IL-23 brings no effect on proliferation of B16F10 cells but can promote invasion which is associated with the increased MMP-9 activities, and this process is correlated with NF-KB signal pathway activation.
出处
《天津医科大学学报》
2014年第1期8-10,13,共4页
Journal of Tianjin Medical University
基金
天津市自然科学基金资助项目(10JCZDJC20400)