[Corrigendum] Curcumin reverses benzidine-induced epithelial-mesenchymal transition via suppression of ERK5/AP-1 in SV-40 immortalized human urothelial cells

• Authors:
  • Zhiqi Liu
  • Jie Liu
  • Li Zhao
  • Hao Geng
  • Jiaxing Ma
  • Zhiqiang Zhang
  • Dexin Yu
  • Caiyun Zhong

• View Affiliations

  
  Affiliations: Department of urology, The Second affiliated Hospital of anhui Medical university, Hefei, Anhui 230032, P.R. China, Department of Nutrition and Food Safety, School of Public Health, Nanjing Medical university, Nanjing, Jiangsu 211166, P.R. China
• Published online on: June 12, 2023     https://doi.org/10.3892/ijo.2023.5533
• Article Number: 85

• Copyright : © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].

Article

Int J Oncol 50: [Related article:] 1321-1329, 2017; DOI: 10.3892/ijo.2017.3887

Following the publication of the above article, an interested reader drew to the authors' attention that, for the Transwell invasion assays shown in Fig. 5D on p. 1326, the images selected for the '0 μM benzidine / 0 μM curcumin' and '0 μM benzidine / 1 μM curcumin' experiments were overlapping, such that these data appeared to have been derived from the same original source. After having consulted their original data, the authors have realized that the '0 μM benzidine / 1 μM curcumin' data panel was selected incorrectly.

Figure 5 Curcumin repairs benzidine-induced SV-HUC-1 EMT via suppression of ERK5/AP-1. (A) Detection of cell viability after treating with curcumin for 4 days, curcumin at concentrations <1 μM had no impact on cell viability. Thus, dose of 1 μM was chosen for consequent experiments. (B) Curcumin attenuated benzidine-induced cell morphology changes. (C) Curcumin reversed benzidine-elevated cell migratory capacity. (D) Treatment with benzidine weakened benzidine-enhanced cell invasive ability as detected by Transwell invasive assay. (E) Cultivation with curcumin leads to elevation of expression levels of E-cadherin and ZO-1 as well as decreased expression levels of vimentin and N-cadherin as determined by western blotting. (F) Cultivation with curcumin upregulated mRNA levels of E-cadherin and ZO-1 and downregulated vimentin and N-cadherin mRNA levels. (G) Curcumin suppressed ERK5/AP-1 activity. Benzidine-induced elevation of phosphorylated ERK5, phosphorylated c-Fos and phosphorylated c-Jun was reversed by curcumin. Data are expressed as mean ± SD. **P<0.01, benzidine groups with control groups. #P<0.05, ##P<0.01, curcumin groups with respective benzidine groups.

The revised version of Fig. 5, showing the correct data for the '0 μM benzidine / 1 μM curcumin' data panel in Fig. 5D, is shown on the next page. The authors regret that this error went unnoticed prior to the publication of this article, and thank the Editor of International Journal of Oncology for allowing them the opportunity to publish this corrigendum. All the authors agree with the publication of this corrigendum; furthermore, they also apologize to the readership of the journal for any inconvenience caused.