CXCL12/CXCR-4对卵巢癌高低转移细胞的作用机制探讨

目的探讨趋化因子CXCL12及其受体CXCR-4对人卵巢浆液性囊腺癌高低转移细胞株HO-8910PM及HO-8910增殖、迁移作用的差异。方法采用流式细胞术分析HO-8910PM及HO-8910细胞中CD44、CD49e、E-cad-herin的表达差异;RT-PCR检测CXCR-4在HO-8910PM及HO-8910细胞中的转录水平差异;比较不同浓度CXCL12对HO-8910PM及HO-8910细胞增殖、迁移能力及对其表面相关黏附分子表达水平的影响。结果流式细胞术检测显示HO-8910PM及HO-8910细胞均表达CD44（97.6%vs 96.2%）,E-cadherin在前者不表达（6.5%）,后者高表达（92.5%）;CXCR-4在HO-8910PM中高表达（93.3%）,在HO-8910中不表达（5.7%）;CXCL12上调HO-8910PM中CD49e的表达（27.6%vs 83.2%,P〈0.05）,并且可促进细胞的增殖和移行。结论趋化因子CXCL12及其受体CX-CR-4在卵巢癌的增殖及侵袭转移中具有重要作用。

Effects of CXCL12/CXCR-4 on proliferation and migration of high and low metastatic human ovarian cancer cells in vitro

Objective To investigate the different effect of chemokine CXCL12 with its receptor CXCR-4 about the biological behavior in high and low metastatic human ovary serous cystadenocarcinoma cells.Methods Expression of adhesion molecules including CD44,CD49e,E-cadherinon on HO-8910PM and HO-8910 ovarian cancer cell lines was determined by flow cytometry.RT-PCR assay was employed to detect the expression of CXCR-4 on both HO-8910PM and HO-8910 cells.The effects of CXCL12,on proliferation,migration and expression of adhesion molecules on those cells were also investigated by MTT,FCM and transwell culture system.Results Expression of CD44(97.6% vs 96.2%) was detected on both HO-8910PM and HO-8910 cells,otherwise,there was almost no expression of E-cadherin on former cells(6.5%),high expression on latter one(92.5%).there was high expression on HO-8910PM cells(93.3%) and almost no expression on HO-8910 cells(5.7%).The adhesion molecules on HO-8910PM was up-regulated in the presence of CXCL12,especially the expression of CD49e(27.6% vs 83.2%,P<0.05).CXCL12 also can induce the proliferation and migration of ovarian cancer cells.Conclusion CXCL 12 and its receptor-CXCR-4 may play a greatly implication on ovarian cancer proliferation and metastasis.