Comparative Expression of RAGE and SOX2 in Benign and Malignant Prostatic Lesions

Document Type : Research Articles

Authors

1 Department of Pathology, Theodor Bilharz Research Institute, Cairo, Egypt.

2 Faculty of Biotechnology, University of Modern Sciences and Arts, Giza, Egypt.

3 Department of Urorology, Theodor Bilharz Research Institute, Cairo, Egypt.

Abstract

Background: Prostate cancer (PCa) is a common health problem in elderly. RAGE (Receptor for advanced glycation
end products) is overexpressed in multiple human cancers. SOX2 (Sex-determining region Y box 2) also functions as an
oncoprotein and promotes cancer progression but the mechanisms involved remain largely unknown. Aim: The current
study investigated the expression patterns of RAGE and SOX2 in benign and malignant prostate samples in correlation
with the histopathological findings in order to evaluate their role as prognostic markers or therapeutic targets. Methods:
Immunohistochemical staining for RAGE and SOX2 antibodies was applied on 87 prostatic biopsies [16 of prostatitis, 20
of benign prostatic hyperplasia (BPH) and 51 of PCa]. Results: Expression of RAGE and SOX2 (percentage of positive
cells) was significantly higher in PCa lesions compared with prostatitis (p<0.01) and BPH (p<0.0001) and was also
significantly higher in prostatitis compared with BPH lesions (p<0.01). Also, percentage of positive RAGE and SOX2
cells showed a significant stepwise increase from Gleason Grade 3 to Grade 5 and were significantly higher in high
Gleason Scores (≥8) compared to lower Scores (≤7) with statistical significance (p=0.001). Conclusion: RAGE and
SOX2 were up-regulated in prostate cancer lesions, mainly in advanced grades, suggesting an active role of both antigens
in the development and progression of prostate cancer and expecting the possibility of their use as therapeutic targets.

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Asian Pacific Journal of Cancer Prevention
Volume 20, Issue 2
February 2019
Pages 615-620

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History

  • Receive Date: 21 September 2018
  • Revise Date: 28 November 2018
  • Accept Date: 20 January 2019

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