Survivin and Cyclooxygenase-2 are co-expressed in human and mouse colon carcinoma and in terminally differentiated colonocytes

Histol Histopathol. 2007 Jan;22(1):61-77. doi: 10.14670/HH-22.61.


In the evolution of colon rectal cancer (CRC) the imbalance between cell proliferation and apoptosis is considered one of the prominent causes of tumor induction and/or progression. In order to establish the role of anti apoptotic proteins in colon cancer development, we studied with immunohistochemical techniques the expression of Survivin in a mouse model of colon carcinogenesis induced by 1,2-dimethyl-hydrazine treatment. In this mouse model Survivin was over-expressed during tumor development, showing a distribution mimicking that described in the correspondent human malignancies. We also correlated Survivin distribution with COX-2 and beta-Catenin expression patterns. The co-localization of COX-2/beta-Catenin/Survivin in the same epithelial cells in tumor samples lends credence to possible in vivo regulatory effects of COX-2 and beta-Catenin on the intracellular Survivin levels in mouse and human colon cancer.

MeSH terms

  • 1,2-Dimethylhydrazine / pharmacology
  • Animals
  • Cell Differentiation
  • Colon / metabolism
  • Colon / pathology*
  • Cyclooxygenase 2 / biosynthesis*
  • Disease Models, Animal
  • Epithelial Cells / cytology
  • Gene Expression Regulation*
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Immunohistochemistry / methods
  • Inhibitor of Apoptosis Proteins
  • Mice
  • Microtubule-Associated Proteins / biosynthesis*
  • Neoplasm Proteins / biosynthesis*
  • Survivin
  • Tissue Distribution
  • beta Catenin / biosynthesis


  • BIRC5 protein, human
  • Inhibitor of Apoptosis Proteins
  • Microtubule-Associated Proteins
  • Neoplasm Proteins
  • Survivin
  • beta Catenin
  • Cyclooxygenase 2
  • 1,2-Dimethylhydrazine