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Copy number changes of CRISP3 in oral squamous cell carcinoma

Wen-Chang Ko1, Keisuke Sugahara, Takumi Sakuma

  • 1Department of Oral and Maxillofacial Surgery, Tokyo Dental College, Mihama, Chiba 261-8502, Japan.

Oncology Letters
|June 29, 2012
PubMed

Insights

Tumor suppressor gene CRISP3 is frequently down-regulated in oral squamous cell carcinoma (OSCC). DNA copy number loss of CRISP3 occurs early in OSCC development, suggesting its role in oral cancer.

Area of Science:

  • Genomics
  • Oncology
  • Molecular Biology

Background:

  • Oral squamous cell carcinoma (OSCC) is a significant global health concern.
  • Identifying novel tumor suppressor genes (TSGs) is crucial for understanding OSCC pathogenesis.
  • Previous studies indicated down-regulation of CRISP3 in OSCC, but its copy number alterations were unexamined.

Purpose of the Study:

  • To identify TSGs in OSCC using whole-genome analysis.
  • To investigate the DNA copy number of the candidate TSG, CRISP3, in OSCC.
  • To determine the potential role of CRISP3 in OSCC development.

Main Methods:

  • Whole-genome analysis of 3 OSCC patient specimens using microarray technology.
  • Real-time quantitative polymerase chain reaction (QPCR) to analyze CRISP3 DNA copy number in 5 OSCC cell lines and 60 OSCC tissues.
  • Statistical analysis to correlate CRISP3 copy number loss with clinical parameters.

Main Results:

  • Microarray analysis identified 11 down-regulated and 2 up-regulated genes in OSCC, with CRISP3 selected for further study.
  • DNA copy number loss of CRISP3 was detected in 40% of OSCC tissues and 2 of 5 cell lines.
  • CRISP3 copy number loss significantly correlated with gender and T classification, indicating an early event in tumorigenesis.

Conclusions:

  • CRISP3 inactivation, evidenced by DNA copy number loss, is an early event in oral squamous cell carcinoma.
  • The findings suggest that CRISP3 functions as a tumor suppressor gene in OSCC.
  • CRISP3 may play a role in the carcinogenesis of oral squamous cell carcinoma.

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