Upregulation of cervical carcinoma expressed PCNA regulatory long non‑coding RNA promotes esophageal squamous cell carcinoma progression

Wang,Xiaojun; Zhou,Liangfen; Zhang,Huiyun; Ou,Hui; Long,Wenxing; Liu,Xiaobao

doi:10.3892/ol.2020.12006

Upregulation of cervical carcinoma expressed PCNA regulatory long non‑coding RNA promotes esophageal squamous cell carcinoma progression

Authors:
- Xiaojun Wang
- Liangfen Zhou
- Huiyun Zhang
- Hui Ou
- Wenxing Long
- Xiaobao Liu
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Affiliations: Department of Oncology, First People's Hospital of Chenzhou City, Chenzhou, Hunan 423000, P.R. China, Department of Neonatology, First People's Hospital of Chenzhou City, Chenzhou, Hunan 423000, P.R. China, Department of Invasive Technology, Affiliated Hospital of Xiangnan College, Chenzhou, Hunan 423000, P.R. China, Department of Oncology, Second People's Hospital of Chenzhou City, Chenzhou, Hunan 423000, P.R. China
Published online on: August 21, 2020 https://doi.org/10.3892/ol.2020.12006
Article Number: 142
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Cervical carcinoma expressed PCNA regulatory long non‑coding (lnc)RNA (CCEPR) has recently been reported to play oncogenic roles in some common types of human cancer. However, the clinical significance of CCEPR mRNA expression levels in esophageal squamous cell carcinoma (ESCC) and the exact function of CCEPR in regulating the malignant phenotypes of ESCC cells have not been previously investigated. In the present study, CCEPR mRNA expression level was upregulated in ESCC tissues and cell lines, and overexpression of CCEPR was associated with advanced TNM stage, lymph node metastasis, and poor prognosis in ESCC. In vitro experiments showed that silencing CCEPR mRNA expression levels significantly suppressed the proliferation, migration, and invasion of ESCC cells, while inducing ESCC cell apoptosis. Furthermore, inhibition of CCEPR decreased the protein expression levels of matrix metalloproteinase (MMP)2 and MMP9 and inhibited epithelial‑mesenchymal transition in ESCC cells. In conclusion, the results showed that CCEPR plays an oncogenic role in ESCC and suggests that CCEPR could be used as a potential therapeutic target for ESCC treatment.

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