[Corrigendum] Receptor for activated C kinase 1 (RACK1) promotes the progression of OSCC via the AKT/mTOR pathway

Zhang,Xuefeng; Liu,Na; Ma,Danhua; Liu,Ling; Jiang,Lu; Zhou,Yu; Zeng,Xin; Li,Jing; Chen,Qianming

doi:10.3892/ijo.2022.5301

February-2022 Volume 60 Issue 2

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[Corrigendum] Receptor for activated C kinase 1 (RACK1) promotes the progression of OSCC via the AKT/mTOR pathway

Authors:
- Xuefeng Zhang
- Na Liu
- Danhua Ma
- Ling Liu
- Lu Jiang
- Yu Zhou
- Xin Zeng
- Jing Li
- Qianming Chen
View Affiliations / Copyright

Affiliations: State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, P.R. China, Department of Oral Diseases, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, P.R. China

Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].
Article Number: 11
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Published online on: January 4, 2022

https://doi.org/10.3892/ijo.2022.5301
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Int J Oncol 49: [Related article:] 539-548, 2016; DOI: 10.3892/ijo.2016.3562

Subsequently to the publication of the above article, an interested reader drew to the authors' attention that Fig. 3 (showing how RACK1 silencing alters the protein expression levels of tumor malignant progress markers in OSCC in vivo) contained an overlapping data panel, such that the data were derived from the same original source where they were intending to depict the results from experiments performed under different experimental conditions and Fig. 4 (showing how RACK1 expression is positively correlated with p-AKT in OSCC tissues and cells) contained a clearly duplicated pair of data panels.

Figure 3

RACK1 silencing changes protein expression levels of tumor malignant progress markers in OSCC in vivo. (A) Percentages of Ki67-positive nuclei in RACK1-sh group were significantly lower than those in the two control groups (mean ± SD, *P<0.05). Angiogenesis in tumors was detected by CD34 and induced VEGF. The average number of microvessels and VEGF expression were significantly lower in RACK1-sh group tissues compared with those in the two control groups (mean ± SD, *P<0.05). (B) RACK1 silence could decrease the expression of RhoA and increase the expression of E-cadherin of OSCC in vivo (mean ± SD, *P<0.05)..

Figure 4

RACK1 expression was positively correlated with p-AKT in OSCC tissues and cells. (A) Protein level of RACK1 and p-AKT have a similar tendency in different stages of oral carcinogenesis tissue. (B) RACK1 expression was positively correlated with p-AKT in OSCC tissues. (C) RACK1 expression was positively correlated with p-AKT in OSCC cells.

The authors were able to re-examine their original data, and have identified the data that were intended to have been shown for these figure parts. The corrected versions of Figs. 3 and 4 are shown on the next two pages, featuring the correct data for the E-cadherin experiments in Fig. 3B and the correct enlargement panel for the RACK1 / Moderate dysplasia experiment in Fig. 4A. The authors confirm that these inadvertent errors did not have any major impact on the conclusions reported in their paper, are grateful to the Editor of International Journal of Oncology for allowing them this opportunity to publish a Corrigendum, and apologize to the readership for any inconvenience caused.

Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

[Corrigendum] Receptor for activated C kinase 1 (RACK1) promotes the progression of OSCC via the AKT/mTOR pathway

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