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Expression and Role of E-Cadherin, β-Catenin, and Vimentin in Human Papillomavirus–Positive and Human Papillomavirus–Negative Oropharyngeal Squamous Cell Carcinoma




TekijätHesham Mohamed, Caj Haglund, Lauri Jouhi, Timo Atula, Jaana Hagström, Antti Mäkitie

KustantajaSAGE PUBLICATIONS LTD

Julkaisuvuosi2020

JournalJournal of Histochemistry and Cytochemistry

Tietokannassa oleva lehden nimiJOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY

Lehden akronyymiJ HISTOCHEM CYTOCHEM

Artikkelin numeroARTN 0022155420950841

Vuosikerta68

Numero9

Aloitussivu595

Lopetussivu606

Sivujen määrä12

ISSN0022-1554

eISSN1551-5044

DOIhttps://doi.org/10.1369/0022155420950841

Rinnakkaistallenteen osoitehttps://research.utu.fi/converis/portal/detail/Publication/50423123


Tiivistelmä
Oropharyngeal squamous cell carcinoma (OPSCC) is subclassified by the World Health Organization into two different entities: human papillomavirus (HPV)-positive and HPV-negative tumors. HPV infection promotes the epithelial-to-mesenchymal transition (EMT) and transformation of keratinocyte stem cells into cancer stem cells. EMT is a crucial process in the carcinogenesis of epithelial-derived malignancies, and we aimed to study the role of its markers in OPSCC. This study consists of 202 consecutive OPSCC patients diagnosed and treated with curative intent. We examined E-cadherin, beta-catenin, and vimentin expression using immunohistochemistry and compared these with tumor and patient characteristics and treatment outcome. We found that the cell-membranous expression of beta-catenin was stronger in HPV-positive than in HPV-negative tumors, and it was stronger in the presence of regional metastasis. The stromal vimentin expression was stronger among HPV-positive tumors. A high E-cadherin expression was associated with tumor grade. No relationship between these markers and survival emerged. In conclusion, beta-catenin and vimentin seem to play different roles in OPSCC: the former in the tumor tissue itself, and the latter in the tumor stroma. HPV infection may exploit the beta-catenin and vimentin pathways in carcinogenic process. More, beta-catenin may serve as a marker for the occurrence of regional metastasis:

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