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| Content Provider | PubMed Central |
|---|---|
| Author | Xu, Yiru Zhou, Jin Carey, Thomas E. Mchugh, Jonathan B. Voorhees, John J. Fisher, Gary J. |
| Copyright Year | 2012 |
| Abstract | Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer and has a high rate of mortality. Emerging evidence indicates that hepatocyte growth factor receptor (or Met) pathway plays a pivotal role in HNSCC metastasis and resistance to chemotherapy. Met function is dependent on tyrosine phosphorylation that is under direct control by receptor-type protein tyrosine phosphatase β (RPTP-β). We report here that RPTP-β expression is significantly downregulated in HNSCC cells derived from metastatic tumors compared to subject-matched cells from primary tumors. Knockdown of endogenous RPTP-β in HNSCC cells from primary tumor potentiated Met tyrosine phosphorylation, downstream mitogen-activated protein (MAP) kinase pathway activation, cell migration, and invasion. Conversely, restoration of RPTP-β expression in cells from matched metastatic tumor decreased Met tyrosine phosphorylation and downstream functions. Furthermore, we observed that six of eight HNSCC tumors had reduced levels of RPTP-β protein in comparison with normal oral tissues. Collectively, the results demonstrate the importance of RPTP-β in tumor biology of HNSCC through direct dephosphorylation of Met and regulation of downstream signal transduction pathways. Reduced RPTP-β levels, with or without Met overexpression, could promote Met activation in HNSCC tumors. |
| Starting Page | 1015 |
| File Format | |
| ISSN | 14765586 |
| e-ISSN | 14765586 |
| Journal | Neoplasia (New York, N.Y.) |
| Issue Number | 11 |
| Volume Number | 14 |
| Language | English |
| Publisher | Neoplasia Press Inc. |
| Publisher Date | 2012-11-01 |
| Access Restriction | Open |
| Rights Holder | Neoplasia Press Inc. |
| Subject Keyword | Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cancer Research |
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