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Article

Methylation of STK11 promoter is a risk factor for tumor stage and survival in clear cell renal cell carcinoma

  • Authors:
    • Fufu Zheng
    • Xiaoxu Yuan
    • Enjing Chen
    • Yunlin Ye
    • Xiaofei Li
    • Yuping Dai
  • View Affiliations / Copyright

    Affiliations: Department of Urology, The First Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China, Department of Urology, Jiangmen Central Hospital, Jiangmen, Guangdong 529030, P.R. China, Department of Urology, Sun Yat‑sen University Cancer Center, Guangzhou, Guangdong 510060, P.R. China
  • Pages: 3065-3070
    |
    Published online on: July 7, 2017
       https://doi.org/10.3892/ol.2017.6534
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Abstract

Inactivation of tumor suppressor gene serine‑threonine kinase 11 (STK11) in clear cell renal cell carcinoma (ccRCC) has been demonstrated; however, the mechanism of this inactivation remains to be investigated. To investigate whether epigenetic alteration plays a role in the inactivation of STK11 in RCC, the present study aimed to investigate the methylation status of the STK11 promoter and its association with tumor stage and survival in ccRCC patients. Paraffin‑embedded specimens were obtained from 42 ccRCC patients. The specimens were analyzed for the methylation status of the STK11 promoter CpG island using methylation‑specific polymerase chain reaction. Survival, tumor‑node‑metastasis (TNM)/American Joint Committee on Cancer (AJCC) stages, and hematological parameters were compared between patients with unmethylated (U), partially methylated (P) and methylated (M) STK11 promoter. Among the 42 patients, there were 12 (28.6%), 18 (42.9%) and 12 (28.6%) patients in the M, P and U groups, respectively. The methylation status of the STK11 promoter was associated with T, N and AJCC stages in RCC. Survival analysis showed that the M group had a significantly shorter survival time compared with the P and U groups. These findings suggested that methylation of the STK11 promoter in RCC is a not rare event, and it may have an important role in the pathogenesis of RCC and be a risk factor for the prognosis of RCC.
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Copy and paste a formatted citation
Spandidos Publications style
Zheng F, Yuan X, Chen E, Ye Y, Li X and Dai Y: Methylation of STK11 promoter is a risk factor for tumor stage and survival in clear cell renal cell carcinoma. Oncol Lett 14: 3065-3070, 2017.
APA
Zheng, F., Yuan, X., Chen, E., Ye, Y., Li, X., & Dai, Y. (2017). Methylation of STK11 promoter is a risk factor for tumor stage and survival in clear cell renal cell carcinoma. Oncology Letters, 14, 3065-3070. https://doi.org/10.3892/ol.2017.6534
MLA
Zheng, F., Yuan, X., Chen, E., Ye, Y., Li, X., Dai, Y."Methylation of STK11 promoter is a risk factor for tumor stage and survival in clear cell renal cell carcinoma". Oncology Letters 14.3 (2017): 3065-3070.
Chicago
Zheng, F., Yuan, X., Chen, E., Ye, Y., Li, X., Dai, Y."Methylation of STK11 promoter is a risk factor for tumor stage and survival in clear cell renal cell carcinoma". Oncology Letters 14, no. 3 (2017): 3065-3070. https://doi.org/10.3892/ol.2017.6534
Copy and paste a formatted citation
x
Spandidos Publications style
Zheng F, Yuan X, Chen E, Ye Y, Li X and Dai Y: Methylation of STK11 promoter is a risk factor for tumor stage and survival in clear cell renal cell carcinoma. Oncol Lett 14: 3065-3070, 2017.
APA
Zheng, F., Yuan, X., Chen, E., Ye, Y., Li, X., & Dai, Y. (2017). Methylation of STK11 promoter is a risk factor for tumor stage and survival in clear cell renal cell carcinoma. Oncology Letters, 14, 3065-3070. https://doi.org/10.3892/ol.2017.6534
MLA
Zheng, F., Yuan, X., Chen, E., Ye, Y., Li, X., Dai, Y."Methylation of STK11 promoter is a risk factor for tumor stage and survival in clear cell renal cell carcinoma". Oncology Letters 14.3 (2017): 3065-3070.
Chicago
Zheng, F., Yuan, X., Chen, E., Ye, Y., Li, X., Dai, Y."Methylation of STK11 promoter is a risk factor for tumor stage and survival in clear cell renal cell carcinoma". Oncology Letters 14, no. 3 (2017): 3065-3070. https://doi.org/10.3892/ol.2017.6534
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