Receptor for activated C kinase 1 (RACK1) promotes the progression of OSCC via the AKT/mTOR pathway
Authors: Lu Jiang
Yu Zhou
Xuefeng Zhang
Xin Zeng
Na Liu
Qianming Chen
Ling Liu
Danhua Ma
Jing Li
Journal: International Journal of Oncology (2016)
Discipline: CLINICAL MEDICINE
Keywords: RACK1; oral squamous cell carcinoma; cell growth; mechanism; in vitro
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.

Abstract:  Our previous study suggested that receptor for activated C kinase 1 (RACK1) contribute to the progression of oral squamous cell carcinoma (OSCC). The aim of this study is to elucidate the mechanism by which RACK1 regulates cell growth in OSCC using in vitro and in vivo models. The effects of RACK1 knockdown with lentivirus based shRNA in stable cell lines were evaluated by Q-PCR and western blot analysis. RACK1 silencing effects on the cell cycle in OSCC cells were detected by flow cytometry and western blot analysis. The effect of RACK1 silencing on inhibiting the progression of OSCC was illustrated using a xenografted mouse model. RACK1 and relevant signaling pathways were investigated in tissues and cells using immunohistochemistry and/or western blot analysis. Stable silencing of the RACK1 gene resulted in a distinct G1 and G2 phase arrest by downregulating Cyclin B1 and Cyclin D1. Depleted RACK1 led to markedly decreased tumor volume and the expression of Ki67, CD34, and VEGF in vivo. The expression of RACK1 and p-AKT has a parallel pattern in different stages of oral carcinogenesis tissues. In addition, the protein level of RACK1 was positively correlated with p-AKT in OSCC tissue samples and cell lines. We found specific transient knockdown of RACK1 could downregulate the protein levels of p-AKT, p-mTOR, and p-S6 in a dose-dependent manner. This study demonstrates that RACK1-dependent OSCC growth and survival may be related to the increased activation of the AKT/mTOR/S6 pathway. 

Retracted: No

PubPeer comments:
 Figure 3. * Red boxes: Two E-cadherin panels appear to show an overlap. ![file] , 
 Figure 4A. * Pink boxes: Two panels appear to look identical. * The green boxes are part of the original figure. ![file] , 
 #1 The E-cadherin IHC staining images in two control groups of Figure 3B (up panel) were mis-placed during the picture assembling, an erratum has been requested to the journal. #2 IHC staining for RACK1 of high magnification in the moderate dysplasia group of Figure 4A was mis-placed during the picture assembling, an erratum has been requested to the journal. , 
 Corrected, [4 January 2022] .  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 pu2011AKT in OSCC tissues and cells) contained a clearly duplicated pair of data panels. The authors were able to reu2011examine 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 Eu2011cadherin 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.  ,