Abstract
Introduction Recent studies show that presenilin 1 may negatively regulate epidermal growth factor receptor expression. Because the epidermal growth factor receptor is frequently over-expressed with limited genetic alterations in head and neck squamous cell carcinoma, we investigated a potential role of presenilin 1 in head and neck squamous cell carcinoma. Methods Presenilin 1 and epidermal growth factor receptor expression levels were measured in head and neck squamous cell carcinoma cell lines and primary tumours using either real-time-polymerase chain reaction and/or immunohistochemistry. Short interfering ribonucleic acid was used to down-regulate presenilin 1 in head and neck squamous cell carcinoma cells to determine its impact on cell growth and epidermal growth factor receptor signaling. Results We found that presenilin 1 was overexpressed in head and neck squamous cell carcinoma cell lines and in 15 of 20 (75%) primary tumours. Surprisingly, presenilin 1 expression was positively associated with epidermal growth factor receptor expression in the tumour tissues (p = 0.0175). Down-regulation of presenilin 1 in head and neck squamous cell carcinoma cells significantly inhibited cell growth by inducing apoptosis. Moreover, the down-regulation resulted in a reduced expression of the epidermal growth factor receptor and inhibited epidermal growth factor receptor down-stream signaling. Conclusion Our data indicated that presenilin 1 is frequently over-expressed in head and neck squamous cell carcinoma. In contrast to the previous reports, our data showed that presenilin 1 is positively related to epidermal growth factor receptor expression in head and neck squamous cell carcinoma and suggested that presenilin 1 may serve as an alternative target for inhibiting epidermal growth factor receptor signaling in head and neck squamous cell carcinoma.
| Original language | English |
|---|---|
| Article number | 47 |
| Journal | Head and Neck Oncology |
| Volume | 4 |
| Issue number | 2 |
| State | Published - Sep 9 2012 |
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