首页 | 本学科首页   官方微博 | 高级检索  
检索        


CIP2A expression and localization in oral carcinoma and dysplasia
Authors:Katz Joseph  Jakymiw Andrew  Ducksworth Monet K  Stewart Carol M  Bhattacharyya Indraneel  Cha Seunghee  Chan Edward K L
Institution:Department of Oral Maxillofacial Surgery and Diagnostic Sciences, University of Florida, College of Dentistry, FL, USA.
Abstract:

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 PP 2A (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 colocalization. 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.Key words: oral cancer, EGFR, CIP2A, dysplasia, C MYC
Keywords:
本文献已被 PubMed 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号