Research Paper Volume 14, Issue 11 pp 4673—4698

CXCR4 knockdown enhances sensitivity of paclitaxel via the PI3K/Akt/mTOR pathway in ovarian carcinoma


Figure 3. Examining effects of CXCR4 knockdown on decreasing the cancer (EOC) invasion capacity. A transwell tumour cell invasion assay showed that knockdown of CXCR4 reduced the invasion ability of OVCA420 cell lines (A) and that overexpression of CXCR4 enhanced the invasion ability of SKOV3 cells (G). The number of invaded cells were quantified by counting the total number of cells from 10 random fields (magnification, 200X) (C, I). A wound-healing assay showed that knockdown of CXCR4 reduced the migration ability of OVCA420 cells (B, D) and that overexpression of CXCRC4 enhanced the migration ability of SKOV3 cells (H, J), respectively. The effects of CXCR4 on the expression of EMT-related E-cadherin, N-cadherin and vimentin protein levels indicated in both CXCR4-knockdown OVCA420 (E) and -overexpressed SKOV3 (K) cell lines were analysed by WB with the indicated antibody against each protein examined, respectively. Band density ratios of each protein indicated to β-actin were determined by densitometry analysis (F, L). Data are presented as the mean ± SD of three independent experiments. Asterisk indicates P<0.05 compared with the controls as determined by t test.