CD105促进卵巢癌细胞转移的机制研究

The mechanism of CD105 promoting metastasis in ovarian cancer

目的:探讨CD105促进卵巢癌上皮细胞转移的机制。方法:通过RNAi技术沉默CD105基因,通过基因芯片对比敲除CD105基因后卵巢癌耐药细胞株中下游靶基因表达变化,利用KEGG数据库对差异基因进行Pathway分析。结果:通过基因芯片对比发现CD105下游调控的靶基因中有意义的是转移抑制因子NDRG1、EMT标记物E-cadherin等基因表达上调,与肿瘤侵袭相关的LncRNA SNHG7显著下调。涉及信号通路有264个,其中有显著性差异(P≤0.05)的信号通路共计27条,与肿瘤代谢、转移、黏附、凋亡的信号通路有Drug metabolism、Cell adhesion molecules(CAMs)、ECM-receptor interaction、MAPK signaling pathway等,并与TGF-β、PI3K-Akt及Jak-STAT通路相关。结论:CD105可能通过抑制NDRG1或促进SNHG7导致卵巢癌的EMT和转移。TGF-β/CD105可能与MAPK/JAK-STAT通路相互作用,导致肿瘤转移。

Objective:To explore the mechanism of CD105 promoting metastasis in ovarian cancer.Methods:CD105 was knockdown by RNAi technology,the gene expression changes in ovarian cancer cells were compared by PCR Microarray.Pathway analysis of differential genes was carried out by KEGG database.Results:The expressions of NDRG1 and E-cadherin were significantly up-regulated,and the expression of LncRNA SNHG7 was significantly down-regulated,which was related to cancer invasiveness.There were 264 signal pathways be involved,with 27 signal pathways had significant differences(P≤0.05).The signal pathways with significant differences involved in tumor metabolism,metastasis,adhesion and apoptosis were as follows:Drug metabolism,Cell adhesion molecules(CAMs),ECM receiver interaction,MAPK signaling pathway,etc.The signal pathways related to CD105 also including the TGF-β,PI3K-Akt and Jak-STAT pathway.Conclusion:CD105 can promote EMT and metastasis of ovarian cancer by inhibiting NDRG1 or promoting LncRNA SNHG7.TGF-β/CD105 may interact with MAPK/JAK-STAT pathway and induce cancer metastasis.