Correction to : Reprod. Sci.

https://doi.org/10.1177/1933719116645192

In the original article, there was an unintended error in Figs. 1C, 4C, and 5C due to unclear image identification during the process of image selection. When the errors were noticed, the authors checked the original data and repeated the Transwell assays again. The results were consistent with the previous. Figures 1, 4, and 5 have now been replaced with the correct pictures of repeated experiments. This change would not affect the conclusion of this paper. The authors all agree to this Correction, and would like to apologize for the inconvenience caused by this error.

Fig. 1
figure 1

Expression of ILK and abilities of migration and invasion in CSCs, EuSCs and EcSCs. (A). Representative western blots showing the expression of ILK in CSCs, EuSCs and EcSCs. (B). Quantitative analysis of ILK expression (**P < 0.005 and ***P < 0.001). The y-axis represents the proportion of protein relative to CSCs. (C). Representative morphology of CSCs, EuSCs and EcSCs (Original magnification, 200 ×); representative transwell migration and invasion assay of CSCs, EuSCs and EcSCs (Original magnification, 200 ×). (D). Quantification of migration abilities of CSCs, EuSCs and EcSCs (**P < 0.005). (E). Quantification of invasion abilities of CSCs, EuSCs and EcSCs (*P < 0.05 and **P < 0.005)

Fig. 4
figure 4

Silencing of ILK in EcSCs induced the MET and decreased migration and invasion abilities of EcSCs. (A). Representative western blots showing the expression of ILK and MET markers in EcSCs after transfection siRNA-ILK with or without the treatment with emodin. (B). Quantitative analysis of ILK and MET markers in EcSCs after transfection siRNA-ILK (EcSCs transfected with N.C. was used as a control: **P < 0.005 and ***P < 0.001) with or without the treatment with emodin (#P < 0.05, ##P < 0.005, and ###P < 0.001). (C). Representative transwell migration and invasion assay of EcSCs after transfection siRNA-ILK with or without the treatment with emodin (Original magnification, 200 ×). (D). Quantification of migration abilities of EcSCs after transfection siRNA-ILK (EcSCs transfected with N.C. was used as a control: **P < 0.005) with or without the treatment with emodin (##P < 0.005). (E). Quantification of invasion abilities of EcSCs after transfection siRNA-ILK (EcSCs transfected with N.C. was used as a control: ***P < 0.001) with or without the treatment with emodin (##P < 0.005)

Fig. 5
figure 5

Exogenous expression of ILK in CSCs induced the EMT and increased migration and invasion abilities of CSCs. (A). Representative western blots showing the expression of ILK and MET markers in CSCs after transfection pEGFP-C1-ILK with or without the treatment with emodin. (B). Quantitative analysis of ILK and MET markers in CSCs after transfection pEGFP-C1-ILK (CSCs transfected with pEGFP-C1 was used as a control: *P < 0.05, **P < 0.005 and ***P < 0.001) with or without the treatment with emodin (##P < 0.005, and ###P < 0.001). (C). Representative transwell migration and invasion assay of CSCs after transfection pEGFP-C1-ILK with or without the treatment with emodin (Original magnification, 200 ×). (D). Quantification of migration abilities of CSCs after transfection pEGFP-C1-ILK (CSCs transfected with pEGFP-C1 was used as a control:**P < 0.005) with or without the treatment with emodin (###P < 0.001). (E). Quantification of invasion abilities of CSCs after transfection pEGFP-C1-ILK (CSCs transfected with pEGFP-C1 was used as a control: *P < 0.05, **P < 0.005 and ***P < 0.001) with or without the treatment with emodin (##P < 0.005)