Long non‑coding RNA RNCR3 promotes glioma progression involving the Akt/GSK‑3β pathway Retraction in /10.3892/ol.2023.14055

Zhu,Bing; Zhang,Shenyan; Meng,Ning; Zhang,He; Yuan,Shaoji; Zhang,Jin

doi:10.3892/ol.2019.11002

Long non‑coding RNA RNCR3 promotes glioma progression involving the Akt/GSK‑3β pathway

Retraction in: /10.3892/ol.2023.14055

Authors:
- Bing Zhu
- Shenyan Zhang
- Ning Meng
- He Zhang
- Shaoji Yuan
- Jin Zhang
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Affiliations: Department of Neurosurgery, Sunshine Union Hospital of Shandong Province, Weifang, Shandong 216000, P.R. China
Published online on: October 18, 2019 https://doi.org/10.3892/ol.2019.11002
Pages: 6315-6322
Copyright: © Zhu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Increasing evidence has confirmed that long non‑coding RNAs (lncRNAs) serve critical roles in the development of a large number of human malignancies, including glioma. Several previously published studies have reported that the lncRNA retinal non‑coding RNA3 (RNCR3; also termed LINC00599) exerts important roles in certain human malignancies; however, the precise biological role and underlying molecular mechanisms of RNCR3 in the development of glioma are yet to be fully elucidated. In the present study, it was revealed that the expression of RNCR3 was increased in glioma tissues compared with in corresponding adjacent normal tissues. Furthermore, increased levels of RNCR3 expression were associated with tumor progression and poor survival rates of patients with glioma. In addition, the U87 and U251 cell lines were selected to investigate the biological function and potential mechanisms of RNCR3 in glioma, and it was observed that RNCR3 knockdown led to an impairment of the proliferative and invasive abilities of cells; furthermore, G1 phase arrest was induced in glioma cells in vitro. Finally, the results of western blot analyses revealed that knockdown of RNCR3 led to a decrease in the expression levels of phosphorylated Akt and glycogen synthase kinase‑3β (GSK‑3β), without any clear effect on the expression levels of total Akt and GSK‑3β. Collectively, these results suggested that RNCR3 is able to regulate cell proliferation, the cell cycle and cell invasion in glioma, potentially via the Akt/GSK‑3β signaling pathway.

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