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Article

Selenium-binding protein 1 is associated with the degree of colorectal cancer differentiation and is regulated by histone modification

  • Authors:
    • Ning Wang
    • Yang Chen
    • Xinghua Yang
    • Yi Jiang
  • View Affiliations / Copyright

    Affiliations: Department of General Surgery, The First Hospital, China Medical University, Shenyang, Liaoning 110001, P.R. China, Central Experimental Laboratory, The First Hospital, China Medical University, Shenyang, Liaoning 110001, P.R. China
  • Pages: 2506-2514
    |
    Published online on: April 16, 2014
       https://doi.org/10.3892/or.2014.3141
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Abstract

The aim of the present study was to examine the regulation of selenium binding protein 1 (SELENBP1) expression in colorectal cancer (CRC). Samples of cancer tissue and adjacent normal mucosa were collected from 83 CRC patients, and analyzed for SELENBP1 expression by 2D-DIGE, immunoblotting, RT-PCR and immunostaining. Expression levels of SELENBP1, carcinoembryonic antigen (CEA) and alkaline phosphatase (AKP) were determined in cultures of human colon cancer cell lines (SW480, SW620 and HT29) folllowing treatment with i) sodium butyrate (NaB, 2 mM), a differentiation inducer; ii) Trichostatin A (TSA, 0.3 µM), a histone deacetylase inhibitor; or iii) 5'-aza-2'-deoxycytidine (5-Aza-dC, 5 µM), a DNA methylation inhibitor. SELENBP1 expression was found to be downregulated (2.54-fold) in the CRC samples as determined by 2D-DIGE and confirmed by immunoblotting and RT-PCR. SELENBP1 expression was correlated with the degree of differentiation, but not with TNM stage or lymph node metastasis, and was higher in benign polyps (1.97±0.57) than in CRC tissues (0.96±0.59). In the CRC cell lines, NaB treatment led to the upregulation of SELENBP1, CEA and AKP when compared with the untreated cells (2.24- to 4.82-fold). SELENBP1 was also upregulated in cells treated with TSA alone (1.25- to 3.64-fold), or in combination with 5-Aza-dC (1.32- to 4.13-fold). In CRC, the downregulated SELENBP1 expression was reactivated by inducing differentiation. Therefore, SELENBP1 is a potential pharmacological target for individualized CRC treatment.
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Copy and paste a formatted citation
Spandidos Publications style
Wang N, Chen Y, Yang X and Jiang Y: Selenium-binding protein 1 is associated with the degree of colorectal cancer differentiation and is regulated by histone modification. Oncol Rep 31: 2506-2514, 2014.
APA
Wang, N., Chen, Y., Yang, X., & Jiang, Y. (2014). Selenium-binding protein 1 is associated with the degree of colorectal cancer differentiation and is regulated by histone modification. Oncology Reports, 31, 2506-2514. https://doi.org/10.3892/or.2014.3141
MLA
Wang, N., Chen, Y., Yang, X., Jiang, Y."Selenium-binding protein 1 is associated with the degree of colorectal cancer differentiation and is regulated by histone modification". Oncology Reports 31.6 (2014): 2506-2514.
Chicago
Wang, N., Chen, Y., Yang, X., Jiang, Y."Selenium-binding protein 1 is associated with the degree of colorectal cancer differentiation and is regulated by histone modification". Oncology Reports 31, no. 6 (2014): 2506-2514. https://doi.org/10.3892/or.2014.3141
Copy and paste a formatted citation
x
Spandidos Publications style
Wang N, Chen Y, Yang X and Jiang Y: Selenium-binding protein 1 is associated with the degree of colorectal cancer differentiation and is regulated by histone modification. Oncol Rep 31: 2506-2514, 2014.
APA
Wang, N., Chen, Y., Yang, X., & Jiang, Y. (2014). Selenium-binding protein 1 is associated with the degree of colorectal cancer differentiation and is regulated by histone modification. Oncology Reports, 31, 2506-2514. https://doi.org/10.3892/or.2014.3141
MLA
Wang, N., Chen, Y., Yang, X., Jiang, Y."Selenium-binding protein 1 is associated with the degree of colorectal cancer differentiation and is regulated by histone modification". Oncology Reports 31.6 (2014): 2506-2514.
Chicago
Wang, N., Chen, Y., Yang, X., Jiang, Y."Selenium-binding protein 1 is associated with the degree of colorectal cancer differentiation and is regulated by histone modification". Oncology Reports 31, no. 6 (2014): 2506-2514. https://doi.org/10.3892/or.2014.3141
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