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目的探讨β-连环蛋白(β-catenin)与卵巢癌转移的相关性及其可能的调节机制。方法采用免疫荧光法、免疫印迹法及反转录-聚合酶链反应(RT-PCR)检测人卵巢浆液性囊腺癌高、低转移细胞系(HO-8910PM及HO-8910)中β-catenin基因的表达差异。为进一步探讨β-catenin调节卵巢癌转移的可能机制,将低转移卵巢癌HO-8910细胞经肝细胞生长因子(HGF)处理,应用上述方法检测β-catenin基因表达的改变;同时经Transwell小室法和划痕实验检测细胞侵袭、迁移能力的改变。结果β-catenin在HO-8910细胞中为高表达,在HO-8910PM细胞中为低表达,差异具有显著性(P<0.05)。HGF可明显降低HO-8910细胞中β-catenin基因的表达(P<0.05)并促进细胞侵袭(P<0.05)和迁移。结论卵巢癌细胞的侵袭、迁移等恶性行为可能与β-catenin基因表达下降有关。经由HGF/c-Met的信号很可能是β-catenin介导的黏附功能的重要调节者。
Objective To investigate the relationship between β-catenin and metastasis of ovarian cancer and its possible regulatory mechanism. Methods The expression of β-catenin in human ovarian serous cystadenocarcinoma cell lines (HO-8910PM and HO-8910) was detected by immunofluorescence, immunoblotting and reverse transcription-polymerase chain reaction Gene expression differences. To further explore the possible mechanism of β-catenin in regulating ovarian cancer metastasis, HO-8910 cells with low metastatic ovarian cancer were treated with hepatocyte growth factor (HGF), and the changes of β-catenin gene expression were detected by the above method. And scratch test to detect cell invasion, migration ability changes. Results β-catenin was highly expressed in HO-8910 cells and low in HO-8910PM cells. The difference was significant (P <0.05). HGF significantly decreased the expression of β-catenin (P <0.05) and promoted cell invasion (P <0.05) and migration in HO-8910 cells. Conclusions The malignant behavior of ovarian cancer cells, such as invasion and migration, may be related to the decrease of β-catenin gene expression. Signals via HGF / c-Met are likely to be important regulators of β-catenin-mediated adhesion function.