Int J Oncol 53: 1069-1082, 2018; DOI: 10.3892/ijo.2018.4482
Subsequently to the publication of the above article and a Corrigendum that addressed the issue of a misspelling of one of the authors' names (DOI: 10.3892/ijo.2019.4769; published online on April 2, 2019), the authors have subsequently discovered that Fig. 7 on p. 1079 contained a duplication in two of the panels that might cause the readers some confusion. The authors were able to re-examine the original data, repeat the experiment, and have decided to revise Fig. 7.
The corrected version of Fig. 7, showing replacement data for the p-Akt and Cyclin D1 experiments, is shown on the next page. The authors confirm that these data continue to support the main conclusions presented in their paper, and are grateful to the Editor of International Journal of Oncology for allowing them this opportunity to publish a Corrigendum. They also apologize to the readership for any inconvenience caused.
LRIG2 enhances the activation of PDGFRβ and regulates its downstream pathways and effectors in vivo. A total of four groups of indicated stable U87 glioblastoma cells (U87-LRIG2, LRIG2 -overexpressing; U87-Con, control U87 cells; U87-LRIG2-sh, LRIG2-knockdown cells; and U87-scr, scramble U87 cells) were injected subcutaneously into the flanks of mice with severe combined immunodeficiency. At the end of the animal experiments, tumor xenografts were isolated and immunohistochemistry was performed to evaluate the expression of LRIG2, PDGFRβ and its downstream pathways, as indicated. Representative images are depicted (scale bars, 20 μm). LRIG2, leucine-rich repeats and immunoglobulin-like domain 2; PDGFRβ, platelet-derived growth factor receptor β.