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

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 retrieve...

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Autores principales: Li, Guangbin, Tong, Xing, Pan, Liangbin, Huang, Haitao, Ma, Haitao, Feng, Yu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7204621/
https://www.ncbi.nlm.nih.gov/pubmed/32391105
http://dx.doi.org/10.3892/ol.2020.11517
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author Li, Guangbin
Tong, Xing
Pan, Liangbin
Huang, Haitao
Ma, Haitao
Feng, Yu
author_facet Li, Guangbin
Tong, Xing
Pan, Liangbin
Huang, Haitao
Ma, Haitao
Feng, Yu
author_sort Li, Guangbin
collection PubMed
description 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=4.19×10(−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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spelling pubmed-72046212020-05-08 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 Oncol Lett Articles 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=4.19×10(−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. D.A. Spandidos 2020-06 2020-04-07 /pmc/articles/PMC7204621/ /pubmed/32391105 http://dx.doi.org/10.3892/ol.2020.11517 Text en Copyright: © Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Li, Guangbin
Tong, Xing
Pan, Liangbin
Huang, Haitao
Ma, Haitao
Feng, Yu
Epididymal protein 3A is upregulated and promotes cell proliferation in non-small cell lung cancer
title Epididymal protein 3A is upregulated and promotes cell proliferation in non-small cell lung cancer
title_full Epididymal protein 3A is upregulated and promotes cell proliferation in non-small cell lung cancer
title_fullStr Epididymal protein 3A is upregulated and promotes cell proliferation in non-small cell lung cancer
title_full_unstemmed Epididymal protein 3A is upregulated and promotes cell proliferation in non-small cell lung cancer
title_short Epididymal protein 3A is upregulated and promotes cell proliferation in non-small cell lung cancer
title_sort epididymal protein 3a is upregulated and promotes cell proliferation in non-small cell lung cancer
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7204621/
https://www.ncbi.nlm.nih.gov/pubmed/32391105
http://dx.doi.org/10.3892/ol.2020.11517
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