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Article

Engrailed‑2 promoter hyper‑methylation is associated with its downregulation in clear cell renal cell carcinoma

  • Authors:
    • Cai‑Yong Lai
    • Gan‑Shen Yu
    • Yin Xu
    • Xun Wu
    • Bao‑Li Heng
    • Yi‑Jun Xue
    • Ze‑Xuan Su
  • View Affiliations / Copyright

    Affiliations: Department of Urology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510632, P.R. China, Department of Urology, The First Affiliated Hospital of Gannan Medical College, Ganzhou, Jiangxi 341000, P.R. China
  • Pages: 6888-6894
    |
    Published online on: September 19, 2017
       https://doi.org/10.3892/ol.2017.7000
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Abstract

In a previous study by the present authors, it was identified that the expression of engrailed‑2 (EN2) gene was downregulated in clear cell renal cell carcinoma (cc‑RCC). The aim of the present study was to determine whether aberrant methylation was the mechanism underlying the silencing of EN2 gene in cc‑RCC. A total of forty paired cc‑RCC tissues, four cc‑RCC cell lines and one normal human proximal tubule epithelial cell line were evaluated for EN2 gene methylation status using methylation‑specific polymerase chain reaction (PCR). Following treatment with 5‑Aza‑dc, reverse transcription‑quantitative PCR and western blot analysis were performed to examine the expression of EN2. Furthermore, cell proliferation, apoptosis and invasion assays were conducted to analyze the inhibitory effects of EN2 re‑expression in 786‑O cells. The results of the present study demonstrated that hyper‑methylation of EN2 was identified in 12/40 cc‑RCC tissues and all cc‑RCC cell lines. The methylation status of the EN2 gene was revealed to be associated with histological grade and tumor size in cc‑RCC. Following 5‑Aza‑dc treatment, demethylation of the EN2 gene was identified in 786‑O cells, in conjunction with EN2 re‑expression. Furthermore, re‑activation of the EN2 gene markedly inhibited the proliferative and invasive capacities of cc‑RCC. The results of the present study demonstrated that the EN2 gene promoter was hyper‑methylated in cc‑RCC, which may underlie the silencing of the EN2 gene in cc‑RCC.
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Copy and paste a formatted citation
Spandidos Publications style
Lai CY, Yu GS, Xu Y, Wu X, Heng BL, Xue YJ and Su ZX: Engrailed‑2 promoter hyper‑methylation is associated with its downregulation in clear cell renal cell carcinoma. Oncol Lett 14: 6888-6894, 2017.
APA
Lai, C., Yu, G., Xu, Y., Wu, X., Heng, B., Xue, Y., & Su, Z. (2017). Engrailed‑2 promoter hyper‑methylation is associated with its downregulation in clear cell renal cell carcinoma. Oncology Letters, 14, 6888-6894. https://doi.org/10.3892/ol.2017.7000
MLA
Lai, C., Yu, G., Xu, Y., Wu, X., Heng, B., Xue, Y., Su, Z."Engrailed‑2 promoter hyper‑methylation is associated with its downregulation in clear cell renal cell carcinoma". Oncology Letters 14.6 (2017): 6888-6894.
Chicago
Lai, C., Yu, G., Xu, Y., Wu, X., Heng, B., Xue, Y., Su, Z."Engrailed‑2 promoter hyper‑methylation is associated with its downregulation in clear cell renal cell carcinoma". Oncology Letters 14, no. 6 (2017): 6888-6894. https://doi.org/10.3892/ol.2017.7000
Copy and paste a formatted citation
x
Spandidos Publications style
Lai CY, Yu GS, Xu Y, Wu X, Heng BL, Xue YJ and Su ZX: Engrailed‑2 promoter hyper‑methylation is associated with its downregulation in clear cell renal cell carcinoma. Oncol Lett 14: 6888-6894, 2017.
APA
Lai, C., Yu, G., Xu, Y., Wu, X., Heng, B., Xue, Y., & Su, Z. (2017). Engrailed‑2 promoter hyper‑methylation is associated with its downregulation in clear cell renal cell carcinoma. Oncology Letters, 14, 6888-6894. https://doi.org/10.3892/ol.2017.7000
MLA
Lai, C., Yu, G., Xu, Y., Wu, X., Heng, B., Xue, Y., Su, Z."Engrailed‑2 promoter hyper‑methylation is associated with its downregulation in clear cell renal cell carcinoma". Oncology Letters 14.6 (2017): 6888-6894.
Chicago
Lai, C., Yu, G., Xu, Y., Wu, X., Heng, B., Xue, Y., Su, Z."Engrailed‑2 promoter hyper‑methylation is associated with its downregulation in clear cell renal cell carcinoma". Oncology Letters 14, no. 6 (2017): 6888-6894. https://doi.org/10.3892/ol.2017.7000
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