[Corrigendum] Downregulation of β3 integrin by miR-30a-5p modulates cell adhesion and invasion by interrupting Erk/Ets‑1 network in triple-negative breast cancer

Int J Oncol 48: [Related article:] 1155-1164, 2016; DOI: 10.3892/ijo.2016.3319

Following the publication of the above paper, an interested reader drew to the authors' attention that, in Fig. 2D, the si-ITGB3/E-cadherin image appeared to show an overlap with the Scr/MDA231+CCL18/N-cadherin image from Fig. 4E in a paper published in 2013 that shared some of the same authors [Zhang B, Yin C, Li H, Shi L, Liu N, Sun Y, Lu S, Liu Y, Sun L, Li X et al: Nir1 promotes invasion of breast cancer cells by binding to chemokine (C-C motif) ligand 18 through the PI3K/Akt/GSK3β/Snail signalling pathway. Eur J Cancer 49: 3900-3913, 2013]. Furthermore, the si-Scb/E-cadherin panel, also featured in Fig. 4D, appeared to show an overlap with a Figure included in the following paper that also featured some of the same authors, published in 2011 [Li W, Liu C, Tang Y, Li H, Zhou F and Lv S: Overexpression of Snail accelerates adriamycin induction of multidrug resistance in breast cancer cells. Asian Pac J Cancer Prev 12: 2575-2580, 2011].

Figure 2 Inhibitory effect on EMT in breast cancer cells by knockdown of β3 integrin. (A) The morphology of MDA-MB-231 cells changed from fibroblastoid to epithelial-like appearance after silencing β3 integrin (upper panel). Downregulation of β3 integrin facilitated the adhesion of MDA-MB-231 cells in vitro (lower panel). (B) Silencing of β3 integrin in MDA-MB-231 resulted in the upregulation of E-cadherin expression and downregulation of Zeb1 expression. Vimentin was assessed by real-time RT-PCR. (C) Western blot analysis was performed to determine E-cadherin, vimentin and Zeb-1 expressions. (D) Fluorescence microscopic staining of E-cadherin and vimentin was performed in MDA-MB-231 cells. Nuclear DNA was stained with DAPI. (E) miR-30a-5p-overexpressing cells exhibited protrusion formation and actin filament destruction compared with uninfected cells. *P<0.05.

The authors were able to re-examine their raw data, and identified the data that should have correctly been used in Fig. 2D in the above paper. The revised version of Fig. 2 is therefore shown on the next page, featuring the correct data panels for the si-Scb/E-cadherin and the si-ITGB3/E-Cadherin experiments. Note that these errors did not have a significant impact on the results or the conclusions reported in this study. The authors are grateful to the Editor of International Journal of Oncology for granting them the opportunity to publish this Corrigendum, and all the authors agree to the publication of this Corrigendum. The authors sincerely apologize for the errors presented in this figure, and apologize to the readership for any inconvenience caused.

Figure 2 Inhibitory effect on EMT in breast cancer cells by knockdown of β3 integrin. (A) The morphology of MDA-MB-231 cells changed from fibroblastoid to epithelial-like appearance after silencing β3 integrin (upper panel). Downregulation of β3 integrin facilitated the adhesion of MDA-MB-231 cells in vitro (lower panel). (B) Silencing of β3 integrin in MDA-MB-231 resulted in the upregulation of E-cadherin expression and downregulation of Zeb1 expression. Vimentin was assessed by real-time RT-PCR. (C) Western blot analysis was performed to determine E-cadherin, vimentin and Zeb-1 expressions. (D) Fluorescence microscopic staining of E-cadherin and vimentin was performed in MDA-MB-231 cells. Nuclear DNA was stained with DAPI. (E) miR-30a-5p-overexpressing cells exhibited protrusion formation and actin filament destruction compared with uninfected cells. *P<0.05.