Epididymal protein 3A is upregulated and promotes cell proliferation in non‑small cell lung cancer

Li,Guangbin; Tong,Xing; Pan,Liangbin; Huang,Haitao; Ma,Haitao; Feng,Yu

doi:10.3892/ol.2020.11517

Epididymal protein 3A is upregulated and promotes cell proliferation in non‑small cell lung cancer

Authors:
- Guangbin Li
- Xing Tong
- Liangbin Pan
- Haitao Huang
- Haitao Ma
- Yu Feng
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Affiliations: Department of Thoracic Surgery, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215000, P.R. China, Department of Pathology, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215000, P.R. China
Published online on: April 7, 2020 https://doi.org/10.3892/ol.2020.11517
Pages: 4024-4030
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Lung cancer is one of the most common cancer types and a major contributor to cancer-associated mortalities worldwide. The aim of the present study was to investigate the function of the epididymal protein 3A (EDDM3A) in non‑small cell lung cancer (NSCLC). Data from patients with NSCLC were retrieved from The Cancer Genome Atlas and analyzed, and the differences in EDDM3A expression level between 30 NSCLC tissues and matched adjacent non‑tumor tissues (>5 cm) were assessed via tissue microarray analysis. It was revealed that, compared with adjacent non‑tumor tissues, EDDM3A expression was significantly increased in NSCLC tissues (P=4.19x10‑2). To knock down EDDM3A expression in a human NSCLC cell line, lentivirus‑mediated short hairpin RNAs (shRNAs) were used, and the knockdown efficiency was assessed via reverse transcription‑quantitative PCR and western blotting. Moreover, cell proliferation was evaluated with an MTT assay and Celigo imaging cytometry. In addition, cell apoptosis was detected by Annexin V staining. It was demonstrated that knockdown of EDDM3A inhibited the proliferation of A549 cells. Furthermore, compared with the control group, the apoptotic rate of the EDDM3A‑shRNA group was significantly higher. Collectively, the present results indicate the potential role of EDDM3A in NSCL and suggest that EDDM3A may represent a potent therapeutic target for treating patients with NSCLC.

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