[Corrigendum] METTL3 antagonizes 5‑FU chemotherapy and confers drug resistance in colorectal carcinoma

• Authors:
  • Min Li
  • Mingyue Xia
  • Ziyu Zhang
  • Yanyin Tan
  • Enjie Li
  • Zhigang Guo
  • Mingzhi Fang
  • Yong Zhu
  • Zhigang Hu

• View Affiliations

  
  Affiliations: Department of Oncology, Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, P.R. China, Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Sciences, Nanjing Normal University, Nanjing, Jiangsu 210023, P.R. China, National Centre of Colorectal Disease, Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, P.R. China
• Published online on: July 24, 2023     https://doi.org/10.3892/ijo.2023.5549
• Article Number: 101

• Copyright : © Li 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 61: [Related article:] 106, 2022; DOI: 10.3892/ijo.2022.5396

Subsequently to the publication of the above article, the authors alerted us to the fact that the data shown in Fig. 8I (for the 'Sh-CN / 0' panel) on p. 11 were mistakenly selected from those data belonging to the experiments shown in Fig. 7H (the 'Sh-CN / 0' panel) of this paper during the final assembly of the figures for review. Note that this error did not affect the conclusions reported in this paper, as both Fig. 7H ('Sh-CN / 0') and Fig. 8I ('Sh-CN / 0') show negative controls of the Comet assay, with no obvious trailing.

Figure 8 Inhibition of RAD51AP1 overcomes 5-FU-resistance in colorectal cancer cells. (A) Western blot analysis of RAD51AP1 in control and RAD51AP1-KD HCT-8R cells. (B) Cell survival assay in control and RAD51AP1-KD HCT-8R cells. (C) Morphological analysis of control and RAD51AP1-KD HCT-8R cells with 60 µg/ml 5-FU treatment for 48 h. (D) Knockdown of RAD51AP1 promotes apoptosis in HCT-8R cells with 5-FU treatment. (E) Silencing of RAD51AP1 induces caspase-3 and Bax expression in HCT-8R cells following 5-FU treatment. (F) Western blotting to determine γ-H2AX levels in control and RAD51AP1-KD HCT-8R cells following 5-FU treatments for 4 h. (G and H) Immunofluorescence staining of γ-H2AX foci and 53BP1 foci in different cells treated 5-FU for 4 h. (I) Comet assay of RAD51AP1-KD and control HCT-8R cells treated with or without 5-FU (60 µg/ml) for 12 h. *P<0.05, **P<0.01 and ***P<0.001. RAD51AP1, RAD51 associated Protein 1; 5-FU, 5-fluorouracil; KD, knockdown; HCT-8R, 5-FU-resistant HCT-8 cells; sh-, small hairpin; CN, control.

The revised version of Fig. 8, showing the correct data for the 'Sh-CN / 0' panel in Fig. 8I, is shown on the next page. The authors are grateful to the Editor of International Journal of Oncology for allowing them this opportunity to publish a Corrigendum, and all the authors agree with its publication. Furthermore, the authors apologize to the readership for any inconvenience caused.