脂氧素类似物BML-111抑制Hela细胞增殖及机制初探

BML-111, the analogue of lipoxin, inhibits Hela cell proliferation

目的:研究脂氧素类似物BML-111对宫颈癌细胞株Hela细胞增殖的影响并进一步探讨其内在机制。方法:分别用50、100、200、400μg/L BML-111刺激Hela细胞,MTT方法检测其对细胞存活率的影响;免疫荧光检测BML-111对Hela细胞P53蛋白表达及细胞定位的影响;Western blot免疫印迹法检测BML-111对Hela细胞NF-κB p65、P53及CyclinD1表达的影响。结果 :与对照组相比,100、200、400μg/L BML-111均能明显降低Hela细胞存活率;免疫荧光显示,BML-111能明显降低P53蛋白的表达,但对细胞定位无影响。Western blot免疫印迹显示,BML-111能明显降低NF-κB p65、P53及CyclinD1蛋白的表达,Boc-2能阻断这种效应。结论:BML-111可以抑制Hela细胞增殖,其作用可能是通过与受体结合,进而抑制NF-κB信号转导途径实现。

Objective To investigate the effect of BML-111 （the analogue of lipoxin） on uterine Hela cell （cervix cancer cell line） proliferation and the underlying mechanism. Methods Hela cells were stimulated by 50, 100, 200 and 400μg/L BML-111, respectively, and cell viability was determined by MTT assay. Hela cells were divided into three groups： the control group （no treatment）, the BML-111 （200 μg/L） group and the BML-111 （200 μg/L）plus Boc-2 （10 μmol/L）group. Expression and location of P53 protein were detected by immunofluorescence. Expressions of NF-κB p65, P53 and CyclinD1 protein were detected by Western blotting. Results BML-111 （100, 200 and 400μg/L） could effectively inhibit Hela cell viability compared with the control group （P 〈 0.05）. P53 expression was shown decreased in both the nucleus and the cytoplasm without any change of P53 location, however, Boc-2 could reverse this effect. BML-111 could effectively inhibit P53 and CyclinD1 expression via NF-κB pathway and the effects could also be inhibited by Boc-2. Conclusions BML-111 can effectively inhibit Hela cell proliferation via FPR2 and NF-KB pathway.