This article has been corrected: The authors replaced the “CXCR4shRNA (#1)/24h” image of the OVCA420 tumor cells used in the transwell invasion assay illustrated in Figure 3A. That image partially overlapped the “CXCR4shRNA (#1)/48h” image due to accidental mislabeling. Replacement was done using a representative image from the “CXCR4shRNA (#1)/24h” group from the original set of experiments.

The authors also corrected Figure 5E (SKOV3 cell invasion induced by CXCR4 overexpression, upper panel), where the control “Scramble” group image of SKOV3 cells was a duplication of the “Scramble” image in Figure 3G. The authors reused the same image because the cells used in Figures 3G (48-hour SKOV3 Scramble group) and 5E (48-hour SKOV3 Scramble group) were from the same batch of experiments. To avoid misinterpretation, the authors have replaced the “Scramble” image in Figure 5E (upper panel) with a representative image from the 48-hour SKOV3 Scramble group from the original set of experiments.

These alterations do not affect the results or conclusions drawn in this work.

Corrected Figures 3 and 5 are presented below.

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

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.

Characterizing the role of the PI3K/Akt/mTOR pathway in promoting CXCR4 overexpression-mediated ovarian cancer invasion, EMT, and CSC stemness. PI3K/Akt/mTOR pathway-related protein phosphorylated states indicated were analysed in both CXCR4 shRNA knockdowned-OVCA420 and CXCR4 overexpressed SKOV3 cells by WB with the indicated antibody against each protein, respectively (A, C). Band density ratios of phosphorylated-PI3K (p-PI3K), -Akt (p-Akt) and -mTOR to total-PI3K (PI3K), -Akt (Akt) and -mTOR (mTOR) were determined by densitometry analysis, respectively (B, D). Effects of MK-2206 on inhibiting SKOV3 cell invasion induced by CXCR4 overexpressing were analysed by a transwell tumour cell invasion assay (E, upper panel). Effects of MK-2206 on inhibiting SKOV3 cell spheroid formation capacity induced by CXCR4 overexpressing were analysed by a spheroid culture in hanging drops assay (E, lower panel), which were quantified by counting the total number of cells (invasion rate) from 10 random fields (magnification, 200X) (F), and the total spheroid hanging drop area (percentage of control) from the CXCR4-overexpressed SKOV3 culture cell experiments, respectively (G). Furthermore, effects of MK-2206 on inhibiting the expression of p-Akt, Akt, EMT-related proteins (E-cadherin, N-cadherin, vimentin and snail) in the CXCR4 overexpressed SKOV3 cells were analysed by WB with the indicated antibody against each protein examined (H). Band density ratios of p-Akt to Akt, E-cadherin, N-cadherin and vimentin to β-actin were determined by densitometry analysis, respectively (I). Data are presented as the mean ± SD of three independent experiments. Asterisk indicates Pt test. Please note that CSC related protein expression profiles in the CXCR4 overexpressed SKOV3 cell line in the presence or absence of MK-2206 treatment were described in the supplementary materials (Supplementary Figure 5).

Figure 5. Characterizing the role of the PI3K/Akt/mTOR pathway in promoting CXCR4 overexpression-mediated ovarian cancer invasion, EMT, and CSC stemness. PI3K/Akt/mTOR pathway-related protein phosphorylated states indicated were analysed in both CXCR4 shRNA knockdowned-OVCA420 and CXCR4 overexpressed SKOV3 cells by WB with the indicated antibody against each protein, respectively (A, C). Band density ratios of phosphorylated-PI3K (p-PI3K), -Akt (p-Akt) and -mTOR to total-PI3K (PI3K), -Akt (Akt) and -mTOR (mTOR) were determined by densitometry analysis, respectively (B, D). Effects of MK-2206 on inhibiting SKOV3 cell invasion induced by CXCR4 overexpressing were analysed by a transwell tumour cell invasion assay (E, upper panel). Effects of MK-2206 on inhibiting SKOV3 cell spheroid formation capacity induced by CXCR4 overexpressing were analysed by a spheroid culture in hanging drops assay (E, lower panel), which were quantified by counting the total number of cells (invasion rate) from 10 random fields (magnification, 200X) (F), and the total spheroid hanging drop area (percentage of control) from the CXCR4-overexpressed SKOV3 culture cell experiments, respectively (G). Furthermore, effects of MK-2206 on inhibiting the expression of p-Akt, Akt, EMT-related proteins (E-cadherin, N-cadherin, vimentin and snail) in the CXCR4 overexpressed SKOV3 cells were analysed by WB with the indicated antibody against each protein examined (H). Band density ratios of p-Akt to Akt, E-cadherin, N-cadherin and vimentin to β-actin were determined by densitometry analysis, respectively (I). 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. Please note that CSC related protein expression profiles in the CXCR4 overexpressed SKOV3 cell line in the presence or absence of MK-2206 treatment were described in the supplementary materials (Supplementary Figure 5).