Author/Authors :
Dai, Yongmei Department of Radiation Oncology, Nanfang Hospital - Southern Medical University, China , Chen, Wenhan The Second Clinical Medical College of Fujian Medical University, China , Huang, Chen Department of Oncology - Provincial Clinical College of Fujian Medical University - Fujian Provincial Hospital, Fujian 350001, China , Luo, Shiyin Department of Oncology - Provincial Clinical College of Fujian Medical University - Fujian Provincial Hospital, China , Huang, Junpeng Department of Oncology - Provincial Clinical College of Fujian Medical University - Fujian Provincial Hospital, China , Xu, Jiangxing Department of General Surgery of the 907th Hospital, Fujian Province, China , Xin, Li Department of Oncology - Provincial Clinical College of Fujian Medical University - Fujian Provincial Hospital, China , Chen, Qianshun Department of Oncology - Provincial Clinical College of Fujian Medical University - Fujian Provincial Hospital, China , Jiang, Guicheng Department of Oncology - Provincial Clinical College of Fujian Medical University - Fujian Provincial Hospital, China , Cui, Tongjian Department of Oncology - Provincial Clinical College of Fujian Medical University - Fujian Provincial Hospital, China , Chen, Longhua Department of Radiation Oncology, Nanfang Hospital - Southern Medical University, China
Abstract :
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.
Keywords :
Proliferation , Nasopharyngeal carcinoma , EMT , EPC1 , Invasion
