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Arch Iran Med. 2021;24(11): 845-851.
doi: 10.34172/aim.2021.125

Scopus ID: 85121054655
  Abstract View: 2134
  PDF Download: 986

Original Article

Expression and Biological Functions of EPC1 in Nasopharyngeal Carcinoma

Yongmei Dai 1,2 ORCID logo, Wenhan Chen 3, Chen Huang 2, Shiyin Luo 2, Junpeng Huang 2, Jiangxing Xu 4, Li Xie 2, Qianshun Chen 2, Guicheng Jiang 2, Tongjian Cui 2, Longhua Chen 1* ORCID logo

1 Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangdong 510515, China
2 Department of Oncology, Provincial Clinical College of Fujian Medical University, Fujian Provincial Hospital, Fujian 350001, China
3 The Second Clinical Medical College of Fujian Medical University, Fujian 362000, China
4 Department of General Surgery of the 907th Hospital, Nanping 353000, Fujian Province, China
*Corresponding Author: *Corresponding Author: Longhua Chen, MD, Professor, Departments of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangdong 510515, China. Tel: 861-13924113168; Email: , Email: chenlh5461@163.com

Abstract

Background: Comb homolog enhancer 1 (EPC1) gene is one of the important members of epigenetic inhibitor PCG family. It shows carcinogenic potential in a variety of malignant tumors, but the expression and role of EPC1 in nasopharyngeal carcinoma are unclear. The aim of this study was to explore the expression and function of enhancer of polycomb homolog 1 (EPC1) in nasopharyngeal carcinoma (NPC).

Methods: The differential expression of EPC1 in the cancer tissues and cell lines of NPC was examined by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). EPC1 expression, cell proliferation, and apoptosis were detected in NPC cell lines after EPC1 silencing, and the levels of the epithelial-mesenchymal transition (EMT)-related proteins E-cadherin and vimentin were detected in NPC cells after EPC1 silencing. The study was performed at Fujian Provincial Hospital, Fujian, China, from 2018 to 2019.

Results: We found that EPC1 was significantly upregulated in the cancer tissues and cell lines of NPC (P<0.001). Furthermore, knockdown of EPC1 inhibited the growth and metastasis of NPC cells. E-cadherin and vimentin were detected in NPC cells after EPC1 was knocked out. It was confirmed that inhibition of EPC1 resulted in increased E-cadherin expression (P<0.001) and decreased vimentin expression (P<0.001), suggesting that inhibition of EPC1 could inhibit the EMT in NPC cells.

Conclusion: EPC1 expression was upregulated in NPC tissues and cell lines. Knockout of EPC1 effectively inhibited the growth of NPC cells, induced apoptosis, and inhibited invasion and metastasis. Inhibition of EPC1 could inhibit the EMT in NPC cells. All of the above findings support the viewpoint that EPC1 plays a pro-cancer role in NPC.



Cite this article as: Dai Y, Chen W, Huang C, Luo S, Huang J, Xu J, et al. Expression and biological functions of epc1 in nasopharyngeal carcinoma. Arch Iran Med. 2021;24(11):845-851. doi: 10.34172/aim.2021.125
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Submitted: 16 Feb 2021
Revision: 17 Apr 2021
Accepted: 21 Apr 2021
ePublished: 01 Nov 2021
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