Long non‑coding RNA CRNDE regulates cell proliferation, migration, invasion, epithelial‑mesenchymal transition and apoptosis in oral squamous cell carcinoma Retraction in /10.3892/ol.2024.14535

Dai,Jing; Mu,Jing‑Wen; Mu,Hong

doi:10.3892/ol.2019.9978

Long non‑coding RNA CRNDE regulates cell proliferation, migration, invasion, epithelial‑mesenchymal transition and apoptosis in oral squamous cell carcinoma

Retraction in 10.3892/ol.2024.14535

Authors:
- Jing Dai
- Jing‑Wen Mu
- Hong Mu
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Affiliations: Department of Stomatology, Jingzhou Central Hospital, The Second Clinical Medical College, Yangtze University, Jingzhou, Hubei 434020, P.R. China, Department of Stomatology, Dongfang Hospital Beijing University of Chinese Medicine, Beijing 100078, P.R. China
Published online on: January 28, 2019 https://doi.org/10.3892/ol.2019.9978
Pages: 3330-3340
Copyright: © Dai et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study aimed to investigate whether the long non‑coding RNA (lncRNA) colorectal neoplasia differentially expressed (CRNDE) can promote the migration and invasion of human oral squamous cell carcinoma (OSCC) cells via the regulation of epithelial‑mesenchymal transition (EMT). CAL‑27 and SCC‑15 cells were classified into a control group, a small interfering negative control (si‑NC) group (cells transfected with control siRNA) and an si‑CRNDE group (cells transfected with CRNDE siRNA). The expression of CRNDE in OSCC tissues and cell lines was detected by in situ hybridization (ISH) and reverse transcription‑quantitative polymerase chain reaction. An MTT assay was used to detect cell proliferation, flow cytometry was performed to determine cell apoptosis, wound‑healing and Transwell assays were conducted to evaluate cell metastasis, and immunofluorescence staining and western blotting were performed to measure the expression of proteins associated with EMT. Tumor‑bearing mouse models were established, and the tumor volumes were recorded. An immunohistochemical assay was performed to determine the expression of EMT‑related proteins. CRNDE expression was increased in OSCC tissues and cell lines compared with that in normal tissues and cell lines. Compared with the control group, the si‑CRNDE group displayed a reduction in the expression of CRNDE, in the proliferation, migration and invasion of cells, in the protein expression of N‑cadherin, vimentin and Snail, and in the expression of proteins in the Wnt/β‑catenin pathway. However, an increase was displayed in the apoptosis of cells and the expression of E‑cadherin. Compared with the control group of tumor‑bearing nude mice, the sh‑CRNDE group demonstrated slowed tumor growth, reduced tumor weight and elevated E‑cadherin, as well as reduced expression of N‑cadherin, vimentin and Snail. In conclusion, silencing CRNDE may inhibit EMT, thus decreasing the migration and invasion of human OSCC cells by repressing the activation of the Wnt/β‑catenin signaling pathway, thereby restricting cell growth and promoting cell apoptosis.

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