Mutational and expressional analyses of STAG2 gene in solid cancers

M S Kim1, S S Kim, E M Je

  • 1Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, Korea.

Neoplasma
|June 7, 2012
PubMed

Insights

Loss of STAG2 protein expression is common in gastric, colorectal, and prostate carcinomas, suggesting it plays a role in cancer development. This loss occurs independently of cancer subtype, stage, or grade, and is not linked to STAG2 gene mutations.

Area of Science:

  • Molecular biology
  • Cancer research
  • Genetics

Background:

  • Aneuploidy is a hallmark of cancer, contributing to tumor development.
  • The STAG2 gene provides instructions for making a protein component of the cohesin complex, essential for accurate chromosome segregation during cell division.
  • Previous studies indicated STAG2 gene mutations and protein loss in glioblastoma, Ewing's sarcoma, and melanoma.

Purpose of the Study:

  • To investigate the frequency of STAG2 gene alterations in various common carcinomas.
  • To determine if STAG2 protein loss is a common event in gastric carcinoma (GC), colorectal carcinoma (CRC), and prostate carcinoma (PCA).

Main Methods:

  • Analyzed STAG2 somatic mutations in 45 GC, 45 CRC, 45 breast carcinomas, 45 non-small cell lung cancers, and 45 prostate carcinomas (PCA) using single-strand conformation polymorphism.
  • Assessed STAG2 protein expression in 100 GC, 103 CRC, and 107 PCA tissues via immunohistochemistry.
  • Compared STAG2 expression in tumor tissues with corresponding normal epithelial cells.

Main Results:

  • STAG2 protein was highly expressed in normal gastric, colon, and prostate epithelial cells.
  • Loss of STAG2 protein expression was observed in 27% of GC, 23% of CRC, and 30% of PCA.
  • No STAG2 gene mutations were detected in the analyzed carcinomas, despite significant protein loss.

Conclusions:

  • Loss of STAG2 protein expression is a frequent event in GC, CRC, and PCA, irrespective of cancer subtype, stage, or grade.
  • The data suggest that STAG2 protein downregulation, rather than somatic mutation, is a common mechanism for STAG2 inactivation in these carcinomas.
  • STAG2 inactivation through protein loss may contribute to aneuploidy and cancer development in these tumor types.