CD105 expression is associated with invasive capacity in ovarian cancer and promotes invasiveness by inhibiting NDRG1 and regulating the epithelial-mesenchymal transition.

This study investigates the association of CD105 (endoglin) with the invasiveness of paclitaxel-resistant ovarian cancer (OC) cells and explores the potential mechanism. A paclitaxel-resistant OC cell line OC3/TAX300, which expresses the stem cell marker CD105 and has a high invasive potential, was established in our previous study. After CD105 knockdown using CD105 siRNA, the invasiveness of the OC cells was decreased, and the chemo-resistance was reversed, but the CD105 overexpression was related to the poor survival of the primary OC patients. The differentially expressed genes were investigated in the OC cells after the CD105 knockdown. The results showed that, in the CD105-siRNA transfected cells, the expressions of some genes (such as KIAA0125, SSTR5-AS1, CDH18, MIAT, NDRG1, E-cadherin, DUSP1, MAL, MYC, and JAK3 ) were significantly upregulated, but the expressions of other genes (such as PRKAR2B, KLK10, DDX17, and lncRNA SNHG7 ) were markedly downregulated. Several genes, such as NDRG1 and E-cadherin, are known to be related to cancer metastasis and the epithelial-mesenchymal transition (EMT). A KEGG analysis found that 264 signaling pathways changed after the CD105 knockdown, of which 27 signaling pathways showed significant enrichment. Our results show that CD105 is related to the metastasis of OC and may promote the EMT of OC by inhibiting NDRG1 and E-cadherin. MYC, JAK3, and IKBKB mediate the CD105-induced metastasis of OC via the MAPK/PI3K/AKT and JAK/STAT signaling pathways in the OC cells. Therefore, inhibiting the CD105 expression may be useful for treating OC.