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August 2012 Volume 28 Issue 2

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Article

Therapeutic targeting of oncogenic transforming growth factor-β1 signaling by antisense oligonucleotides in oral squamous cell carcinoma

  • Authors:
    • Seong-Gon Kim
    • Ji-Young Song
  • View Affiliations / Copyright

    Affiliations: Department of Oral and Maxillofacial Surgery, College of Dentistry, Gangneung-Wonju National University, Gangneung 210-702, Republic of Korea
  • Pages: 539-544
    |
    Published online on: May 10, 2012
       https://doi.org/10.3892/or.2012.1811
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Abstract

The transforming growth factor-β1 (TGF-β1) signaling pathway is important in human oral squamous cell carcinoma (OSCC). Accordingly, the aims of this study were to evaluate the effect of antisense TGF-β1 oligonucleotides (ODNs) on OSCC in cell culture and in a xenograft model, as well as to evaluate any effects ODNs have on proliferating cell nuclear antigen (PCNA) and matrix metalloproteinase-2 (MMP-2) expression in the xenograft model. We performed real-time cell electronic sensing (RT-CES) to determine the effect of antisense TGF-β1 ODNs on SCC-9 cell growth. To examine the in vivo effect of antisense TGF-β1 ODN therapy, SCC-9 cells were grafted into nude mice. Antisense ODNs were injected into the mass daily. Tumor size, body weight and duration of survival were assessed daily. Specimens from the main mass were used for immunohistochemical staining to analyze PCNA and MMP-2 expression. In vitro treatment with antisense TGF-β1 ODNs decreased TGF-β1 expression and growth of SCC-9 cells. In the xenograft model, the antisense TGF-β1 ODN group exhibited a significantly decreased tumor growth rate compared to the control, which received Dulbecco's modified Eagle's medium (DMEM) (P=0.022). However, mean survival time and body weights were not significantly different between the groups (P>0.05). Immunohistochemistry showed that tumors from animals that received antisense TGF-β1 ODNs had significantly lower expression levels of PCNA and MMP-2 compared to tumors from animals in the DMEM group (P<0.05). In conclusion, antisense TGF-β1 ODN therapy significantly inhibits tumor growth compared to controls, however, there are no significant differences between groups with respect to changes in body weight.
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Copy and paste a formatted citation
Spandidos Publications style
Kim S and Song J: Therapeutic targeting of oncogenic transforming growth factor-β1 signaling by antisense oligonucleotides in oral squamous cell carcinoma. Oncol Rep 28: 539-544, 2012.
APA
Kim, S., & Song, J. (2012). Therapeutic targeting of oncogenic transforming growth factor-β1 signaling by antisense oligonucleotides in oral squamous cell carcinoma. Oncology Reports, 28, 539-544. https://doi.org/10.3892/or.2012.1811
MLA
Kim, S., Song, J."Therapeutic targeting of oncogenic transforming growth factor-β1 signaling by antisense oligonucleotides in oral squamous cell carcinoma". Oncology Reports 28.2 (2012): 539-544.
Chicago
Kim, S., Song, J."Therapeutic targeting of oncogenic transforming growth factor-β1 signaling by antisense oligonucleotides in oral squamous cell carcinoma". Oncology Reports 28, no. 2 (2012): 539-544. https://doi.org/10.3892/or.2012.1811
Copy and paste a formatted citation
x
Spandidos Publications style
Kim S and Song J: Therapeutic targeting of oncogenic transforming growth factor-β1 signaling by antisense oligonucleotides in oral squamous cell carcinoma. Oncol Rep 28: 539-544, 2012.
APA
Kim, S., & Song, J. (2012). Therapeutic targeting of oncogenic transforming growth factor-β1 signaling by antisense oligonucleotides in oral squamous cell carcinoma. Oncology Reports, 28, 539-544. https://doi.org/10.3892/or.2012.1811
MLA
Kim, S., Song, J."Therapeutic targeting of oncogenic transforming growth factor-β1 signaling by antisense oligonucleotides in oral squamous cell carcinoma". Oncology Reports 28.2 (2012): 539-544.
Chicago
Kim, S., Song, J."Therapeutic targeting of oncogenic transforming growth factor-β1 signaling by antisense oligonucleotides in oral squamous cell carcinoma". Oncology Reports 28, no. 2 (2012): 539-544. https://doi.org/10.3892/or.2012.1811
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