4.5 Article

CIP2A expression and localization in oral carcinoma and dysplasia

Journal

CANCER BIOLOGY & THERAPY
Volume 10, Issue 7, Pages 694-699

Publisher

TAYLOR & FRANCIS INC
DOI: 10.4161/cbt.10.7.12895

Keywords

oral cancer; EGFR; CIP2A; dysplasia; C MYC

Categories

Funding

  1. UFCD
  2. NIDCR [T32 DE007200, K99DE018191]
  3. NIH [AI47859]
  4. Bankhead-Coley Cancer Research Program
  5. Florida Department of Health [08BN-02]
  6. Andrew J. Semesco Foundation
  7. Micromedic Tech

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Aims: Oral squamous cell carcinoma (OSCC) is the most prevalent malignancy of the oral cavity resulting in severe morbidity and mortality. To date only few proteins have been suggested as potential biomarkers or targets for this type of cancer. Cancerous inhibitor of PP2A (CIP2A) is a protein expressed in epithelial tissues that stabilizes the oncogene c-Myc and causes cell transformation. This study was designed to investigate the expression of CIP2A in OSCC cell lines and tissues representing human normal, dysplasia and OSCC. Results: CIP2A was significantly increased in the human carcinoma cell lines compared to the primary gingival cell line. CIP2A was overexpressed in the human oral dysplasia and OSCC tissues compared to normal oral tissues. CIP2A was also preferentially localized in the dysplastic and OSCC epithelial areas compared to EGFR that was expressed mainly in areas of relatively normal epithelium and in dysplastic tissues above the basal layers. Methods: Using quantitative real time PCR, mRNA quantification for CIP2A was performed in a primary gingival cell line and OSCCs CAL 27 and SCC-25. Paraffin embedded human specimen classified as normal, dysplastic or OSCC were immunohistochemically stained for CIP2A expression. EGFR and CIP2A were also stained by immunofluorescence for co-localization. Samples of human normal oral tissue and OSCC were studied by PCR for mRNA expression of CIP2A. Conclusions: CIP2A may play a significant role in oral malignant transformation and therefore, it may be a potential target for chemotherapy of OSCC.

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