Tid1 functions as a tumour suppressor in head and neck squamous cell carcinoma |
| |
| Authors: | Chi‐Yuan Chen Shih‐Hwa Chiou Chih‐Yang Huang Chia‐Ing Jan Shu‐Chun Lin Wen‐Yuan Hu Shiu‐Huey Chou Chung‐Ji Liu Jeng‐Fan Lo |
| |
| Affiliation: | 1. Institute of Oral Biology, National Yang‐Ming University, Taipei, Taiwan, ROC;2. Department of Medical Research and Education, Taipei Veterans General Hospital, Taipei, Taiwan, ROC;3. Graduate Institute of Chinese Medical Science and Institute of Medical Science, China Medical University, Taichung, Taiwan, ROC;4. Institute of Basic Medical Science, China Medical University, Taichung, Taiwan, ROC;5. Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan, ROC;6. Department of Pathology, China Medical University and Hospital, Taichung, Taiwan, ROC;7. Biosettia Inc, San Diego, CA, USA;8. Department of Life Science, Fu‐Jen University, Taipei, Taiwan, ROC;9. Department of Oral and Maxillofacial Surgery, Mackay Memorial Hospital, Taipei, Taiwan, ROC |
| |
| Abstract: | Human tumourous imaginal disc (Tid1), a human homologue of the Drosophila tumour suppressor protein Tid56, is involved in multiple intracellular signalling pathways such as apoptosis, cell proliferation, and cell survival. Here, we investigated the anti‐tumourigenic activity of Tid1 in head and neck squamous cell carcinoma (HNSCC) in vitro and in vivo. Firstly, the clinical association between Tid1 expression and progression of HNSCC was explored. It was found that expression of Tid1 was negatively associated with tumour status, recurrence, and survival prognosis using immunohistochemical analysis of primary HNSCC patient tumour tissue. Secondly, ectopic expression of Tid1 in HNSCC cells was shown to significantly inhibit cell proliferation, migration, invasion, anchorage‐independent growth, and xenotransplantation tumourigenicity. Thirdly, we showed that overexpression of Tid1 attenuated EGFR activity and blocked the activation of AKT in HNSCC cells, which are known to be involved in the regulation of survival in HNSCC cells. On the other hand, ectopic expression of constitutively active AKT greatly reduced apoptosis induced by Tid1 overexpression. Together, these findings suggest that Tid1 functions as a tumour suppressor in HNSCC tumourigenesis. Copyright © 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |
| |
| Keywords: | Tid1 head and neck cancer EGFR AKT tumour suppressor |
|
|
