LncRNA FOXP4-AS1 silencing inhibits metastasis and epithelial–mesenchymal transition in nasopharyngeal carcinoma via miR-136-5p/MAPK1: Erratum

The authors have identified errors in two figures in their paper [1]. The representative images supplied for the Transwell experiments shown in Fig. 3b for the FOXP4-AS1-siRNA group and Fig. 6b for the miR-136-5p mimic group were incorrect. New images for Fig. 3b and 3d, and Fig. 6b and 6d from replicate experiments are provided and the revised figures appear below. These changes do not affect the conclusions of this study.

Fig. 3.

Effects of FOXP4-AS1-siRNA or miR-136-5p inhibitor on NPC cells viability, migration, invasion, and EMT. (a) Cell viability was measured by MTT assay. Transwell was applied for analyzing (b and c) cell invasion and (d and e) migration. (f) Western blot analysis of E-cadherin and N-cadherin was detected. mRNA level of (g) E-cadherin and (h) N-cadherin in C666-1 cells. ^**P<0.01 vs. Control-plasmid; ##P<0.01 vs. FOXP4-AS1-siRNA+inhibitor control. EMT, epithelial–mesenchymal transition; NPC, nasopharyngeal carcinoma.

Fig. 6.

MAPK1-plasmid reversed the effects of miR-136-5p mimic on NPC cells viability, migration, invasion and EMT. (a) Cell viability was measured by MTT assay. Transwell was applied for analyzing (b and c) cell invasion and (d and e) migration. (f) Western blot analysis of E-cadherin and N-cadherin was detected. mRNA level of (g) E-cadherin and (h) N-cadherin in C666-1 cells. ^**P<0.01 vs. Mimic control; ##P<0.01 vs. miR-136-5p mimic+control-plasmid. EMT, epithelial–mesenchymal transition; NPC, nasopharyngeal carcinoma.