Higher expression of WNT5A protein in oral squamous cell carcinoma compared with dysplasia and oral mucosa with a normal appearance.
Eur J Oral Sci
; 125(4): 237-246, 2017 08.
Article
en En
| MEDLINE
| ID: mdl-28603941
ABSTRACT
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, ß-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 ß-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 ß-catenin and of E-cadherin was lower, whereas expression of cytoplasmic ß-catenin was higher, in OSCCs than in non-cancerous regions. However, there was no correlation between expression of WNT5A and expression of either ß-catenin or E-cadherin. Furthermore, treatment of OSCC cells with rWNT5A had no effect on the expression of ß-catenin or E-cadherin. Taken together with previous results, we conclude that WNT5A influences the progression of OSCC without affecting the canonical WNT/ß-catenin pathway and without down-regulating E-cadherin. WNT5A may have potential as a biological marker for malignant transformation of dysplasia to OSCC.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Lesiones Precancerosas
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Neoplasias de la Boca
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Carcinoma de Células Escamosas
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Proteína Wnt-5a
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Mucosa Bucal
Límite:
Adult
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Aged
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Eur J Oral Sci
Asunto de la revista:
ODONTOLOGIA
Año:
2017
Tipo del documento:
Article
País de afiliación:
Suecia