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Corrigendum

RANKL/RANK Pathway Abrogates Cetuximab Sensitivity in Gastric Cancer Cells via Activation of EGFR and c-Src [Corrigendum]

Pages 529-530 | Published online: 13 May 2022
This article refers to:
RANKL/RANK pathway abrogates cetuximab sensitivity in gastric cancer cells via activation of EGFR and c-Src

Zhang X, Song Y, Song N, et al. Onco Targets Ther. 2017;10:73–83.

In a detailed re-analyses of the data post-publication, the authors found the incorrect images were used for on page 80. Due to an error at the time of figure assembly the images from was used as a placeholder and not replaced later. The correct is shown below.

The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way.

Figure 5 Continued.

Figure 5 Continued.

Figure 5 The effect of dasatinib on RANKL-induced cetuximab resistance in SGC-7901 cells.

Notes: (A and B) SGC-7901 and MGC-803 cells were treated with 100 nM dasatinib or 10 μM PP2 for the indicated times. Expression of c-Src, EGFR, AKT, and ERK and phosphorylation levels were analyzed by Western blot. (C) SGC-7901 cells were treated with 100 nM dasatinib for 24 hours, followed by 1 μg/mLsRANKL for 1 hour and then 10 μg/mL cetuximab for 48 hours. The cell viability was assessed by MTT assay. *Comparisons between the cetuximab-treated cells and the combined-treated cells in the control arm, P<0.05. (D) SGC-7901 cells were treated with or without 100 nM dasatinib for 2 hours and then preincubated with 1 μg/mLs RANKL for 1 hour, followed by 10 μg/mL cetuximab for 48 hours. The expression of c-Src, EGFR, AKT, and ERK and phosphorylation levels were analyzed by Western blot.
Figure 5 The effect of dasatinib on RANKL-induced cetuximab resistance in SGC-7901 cells.