期刊
EUROPEAN JOURNAL OF ORAL SCIENCES
卷 125, 期 4, 页码 237-246出版社
WILEY
DOI: 10.1111/eos.12352
关键词
E-cadherin; immunohistochemistry; oral cancer; WNT5A; beta-catenin
资金
- Swedish Cancer Foundation
- Swedish Research Council
- Skane University Hospital Research Foundations
- Gunnar Nilsson's Cancer Foundation
- Malmo Allmanna Sjukhus Cancer Foundation
WNT5A is a secreted signaling protein that promotes migration and invasion of oral squamous cell carcinoma (OSCC) cells through activation of non-canonical WNT signaling. Here, we examined expression of WNT5A, beta-catenin, and E-cadherin by immunohistochemistry in 21 human diagnostic incision biopsies that each had regions of oral mucosa with a normal appearance adjacent to the affected tissue, dysplasia, and OSCC. We also investigated the effect of recombinant WNT5A (rWNT5A) on expression of the cell-adhesion proteins E-cadherin and beta-catenin by western blot analysis. No expression of WNT5A protein was present in oral mucosa with a normal appearance or in mild grade dysplasia. However, expression of WNT5A increased along with increasing grade of dysplasia, and the highest expression was detected in OSCCs. Expression of membranous beta-catenin and of E-cadherin was lower, whereas expression of cytoplasmic beta-catenin was higher, in OSCCs than in non-cancerous regions. However, there was no correlation between expression of WNT5A and expression of either beta-catenin or E-cadherin. Furthermore, treatment of OSCC cells with rWNT5A had no effect on the expression of beta-catenin or E-cadherin. Taken together with previous results, we conclude that WNT5A influences the progression of OSCC without affecting the canonical WNT/beta-catenin pathway and without down-regulating E-cadherin. WNT5A may have potential as a biological marker for malignant transformation of dysplasia to OSCC.
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