Overexpression of CC3/TIP30 is associated with HER-2/neu status in breast cancer

J Cancer Res Clin Oncol. 2005 Sep;131(9):603-8. doi: 10.1007/s00432-005-0674-z. Epub 2005 Oct 20.

Abstract

Purpose: The human CC3/TIP30 gene is a putative metastasis suppressor gene, based on the results of experimental studies using lung, colon and melanoma cell lines. However, there is very little evidence from studies on clinical material, in support of such a role for the gene. In this study, we evaluated the expression of CC3/TIP30 in human breast cancer tissue and investigated the possible associations with the clinicopathological parameters.

Methods: Total RNA and proteins were extracted from the frozen breast tumor and matched normal tissues. Evaluation of CC3/TIP30 expression was assessed by reverse transcription (RT)-PCR and reverse phase protein array. Immunohistochemistry of CC3/TIP30 on breast tissue microarrays was also analyzed.

Results: We have found that CC3/TIP30 expression is significantly associated with positive HER-2/neu status at both mRNA (P=0.023) and protein (P=0.016) levels. Immunohistochemical analysis on tissue microarrays also shows a positive correlation between CC3 expression and HER-2/neu status (P=0.0028).

Conclusion: Our findings suggest a potential link between the expression of CC3/TIP30 gene and the HER-2/neu oncogene-mediated signal pathway.These findings could not have been predicted from previous experimental studies, and suggest that CC3/TIP30 may play a complex role in breast cancer.

MeSH terms

  • Acetyltransferases / biosynthesis*
  • Acetyltransferases / genetics
  • Amino Acid Sequence
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Cytoplasm / metabolism
  • DNA, Complementary / analysis
  • Female
  • Gene Expression
  • Humans
  • Immunohistochemistry
  • Protein Array Analysis
  • Receptor, ErbB-2 / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transcription Factors / biosynthesis*
  • Transcription Factors / genetics

Substances

  • DNA, Complementary
  • Transcription Factors
  • Acetyltransferases
  • HTATIP2 protein, human
  • Receptor, ErbB-2