基质细胞衍生因子-1α促进乳腺癌细胞侵袭和转移

Promotion of invasion and metastasis in human breast carcinoma MCF-7 by SDF-1α

背景与目的:根据基质细胞衍生因子1α(SDF-1α)/CXCR4生物学轴的多种生物学功能,本实验在研究CXCR4内化及其调变的基础上,进一步探讨SDF-1α对乳腺癌细胞体外侵袭转移能力的影响。方法:应用细胞黏附实验、细胞迁徙实验及失巢凋亡实验对比分析SDF-1α对乳腺癌MCF-7细胞形态、体外黏附能力、迁徙能力及抗失巢凋亡能力的影响。结果:与SDF-1α共培养的乳腺癌MCF-7细胞形态变为长梭形,伪足更长而伸展,其黏附能力高于MCF-7细胞株[(0.90±0.18)vs(0.68±0.08),P<0.01];侵袭小室实验发现,与SDF-1α共培养的MCF-7细胞侵袭转移能力增强,培养6h迁徙进入微孔膜的细胞数比MCF-7细胞株明显增多[(151±11)比(135±13),P<0.01]。悬浮培养的SDF-1α加MCF-7细胞比MCF-7细胞更容易聚集,形成相对较致密的细胞团块,24h检测流式细胞凋亡指数下降[(9.1±1.1)%vs(18.4±1.7)%,P<0.01]。结论:SDF-1α可明显增强乳腺癌细胞MCF-7体外侵袭及转移能力。

Background and purpose： We have already reported viral macrophage inflammatory protein- Ⅱ can induce surface chemokine receptor CXCR4 intemalizated. Based on the diverse biological functions of SDF-1α/ CXCR4, this study was to investigate the effect of SDF-1α on invasion and metastasis of human breast carcinoma MCF-7 cells. Methods： MCF-7 cell＇s ability of invasion,metastasis and anoikis were used as end points. The invasive ability was measured by the number of cells that were able to penetrate polycarbonates coated with matrigel.The metastastatic ability was analyzed by Transwell chamber.The anoikis ability was detected by FCM. Results： SDF- 1α＋ MCF-7 cells formed long and abundant pseudopodia, and only few filopodia were detectable in MCF-7 cells. It was shown that adhesive and metastasis capability of MCF-7 cells was enhanced with SDF-1α cocultured （P〈0.01）. Apoptosis index of SDF-1α＋ MCF-7 group, because of loss of cell-matrix interactions, decreased as compared with pure MCF-7 group（P〈0.01）. Conclusions： SDF-1α significantly elevates the capacity in terms of the invasion and metastasis of breast carcinoma MCF-7 cells.