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Analytical Cellular Pathology
Volume 33, Issue 5-6, Pages 177-189

The Survivin −31 Snp in Human Colorectal Cancer Correlates with Survivin Splice Variant Expression and Improved Overall Survival

Anna G. Antonacopoulou,1 Konstantina Floratou,1 Vasiliki Bravou,1,2 Anastasia Kottorou,1 Fotinos-Ioannis Dimitrakopoulos,1 Stella Marousi,1 Michalis Stavropoulos,3 Agelos K. Koutras,1 Chrisoula D. Scopa,4 and Haralabos P. Kalofonos1

1Molecular Oncology Laboratory, Medical School, University of Patras, Rion, Greece
2Department of Anatomy–Histology–Embryology, Medical School, University of Patras, Rion, Greece
3Department of Surgery, Medical School, University of Patras, Rion, Greece
4Department of Pathology, Medical School, University of Patras, Rion, Greece

Copyright © 2010 Hindawi Publishing Corporation and the authors. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background: Survivin is involved in the regulation of cell division and survival, two key processes in cancer. The majority of studies on survivin in colorectal cancer (CRC) have focused on protein expression and less is known about the expression of survivin splicing variants or survivin gene polymorphisms in CRC. In the present study, the mRNA levels of the five known isoforms of survivin as well as survivin protein were assessed in matched normal and neoplastic colorectal tissue. Moreover, the 9386C/T and −31G/C polymorphisms were investigated.

Methods: Quantitative RT-PCR was used to assess mRNA levels in fresh/frozen tissue samples. Protein levels were immunohistochemically evaluated on formalin-fixed paraffin-embedded tissue sections. Individuals were genotyped using real time PCR.

Results: Expression of all 5 survivin splice variants as well as survivin protein was elevated in colorectal carcinomas compared to normal tissue. Specific splice variant expression differentially correlated with clinicopathological parameters. Furthermore, both snps correlated with splice variant levels or their ratios in colorectal carcinomas while the −31G/C snp may be related to CRC development and improved overall survival.

Conclusion: Our results support a role of survivin in colorectal carcinogenesis while the −31G/C snp may constitute a marker of survival.