Upregulation of discoidin domain receptor 2 in nasopharyngeal carcinoma
Autor: | Ching-Hwa Tsai, You Chang Lo, Ying Piao Wang, Huey Huey Chua, Tzung Shiahn Sheen, Te-Huei Yeh, Ya Ching Chou, Yu Tzu Huang |
---|---|
Rok vydání: | 2008 |
Předmět: |
Transcription
Genetic Nasopharyngeal neoplasm Polymerase Chain Reaction Viral Proteins Downregulation and upregulation Gene expression otorhinolaryngologic diseases medicine Humans Lymphocytes Discoidin Domain Receptors DDR1 Reporter gene business.industry Carcinoma Receptor Protein-Tyrosine Kinases Epithelial Cells Nasopharyngeal Neoplasms medicine.disease Immunohistochemistry Up-Regulation Gene Expression Regulation Neoplastic stomatognathic diseases Otorhinolaryngology Nasopharyngeal carcinoma Receptors Mitogen Trans-Activators Cancer research business Tyrosine kinase Discoidin domain |
Zdroj: | Head & Neck. 30:427-436 |
ISSN: | 1097-0347 1043-3074 |
DOI: | 10.1002/hed.20724 |
Popis: | Background. Nasopharyngeal carcinoma (NPC) is associated with Epstein-Barr virus (EBV) and has high meta- static potential. Discoidin domain receptors (DDR1, DDR2) are receptor-type tyrosine kinases activated by collagen. Their abil- ity to induce expression of matrix metalloproteinase is related with tumor invasion. Therefore, we aim to investigate DDRs gene expression and its regulation in NPC. Methods and Results. By use of real-time quantitative poly- merase chain reaction (Q-PCR), DDR2 gene expression but not DDR1 was significantly higher in primary and metastatic NPC. DDR2 was predominantly distributed in NPC tumor cells rather than in infiltrating lymphocytes. EBV Z-transactivator (Zta) trans- fection may distinctly elevate DDR2 level. Furthermore, data from reporter assay indicate that Zta could transactivate DDR2 pro- moter activity, suggesting the possible upregulation mechanism. Conclusion. DDR2 was differentially upregulated in NPC and modulated by EBV Zta protein. DDR2 may play a role in NPC invasion and serve as a diagnostic and therapeutic target. |
Databáze: | OpenAIRE |
Externí odkaz: |