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Nuclear nonmetastatic protein 23‐H1 expression and epithelial‐mesenchymal transition in laryngeal carcinoma: A pilot investigation
Author(s) -
Marioni Gino,
Cappellesso Rocco,
Ottaviano Giancarlo,
Fasanaro Elena,
MarcheseRagona Rosario,
Favaretto Niccolò,
Giacomelli Luciano,
Guzzardo Vincenza,
Martini Alessandro,
Fassina Ambrogio,
Blandamura Stella
Publication year - 2018
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.25188
Subject(s) - epithelial–mesenchymal transition , immunohistochemistry , mesenchymal stem cell , cancer research , nuclear protein , cadherin , zinc finger , pathology , carcinoma , biology , oncology , cell , medicine , metastasis , cancer , transcription factor , gene , biochemistry , genetics
Background In epithelial‐to‐mesenchymal transition, epithelial cells lose their features, acquiring a mesenchymal‐like phenotype. Nm23‐H1 protein relates to tumor cells' metastatic potential, its low expression in carcinomas often meaning a poor prognosis. This study newly investigated the role of nuclear nm23‐H1 in laryngeal squamous cell carcinoma epithelial‐to‐mesenchymal transition. Methods Immunohistochemical analyses of nuclear nm23‐H1, E‐cadherin, N‐cadherin, Snail, Zinc finger E‐box binding homeobox (ZEB)1, and ZEB2 were performed in 33 consecutive patients with laryngeal SCC. Results Mean nuclear nm23‐H1 expression was lower in patients whose disease recurred ( P = .0046). Disease‐free survival (DFS) was longer for patients whose nuclear nm23‐H1 expression was ≥10% ( P = .0083). Nuclear nm23‐H1 and E‐cadherin expressions correlated directly ( P = .018). Mean E‐cadherin expression was lower in patients whose disease recurred ( P = .03). The DFS was shorter in patients with ZEB2 expression ≥5% ( P = .006). Conclusions Nuclear nm23‐H1 expression warrants further investigation in laryngeal SCC as a prognostic marker identifying patients at higher risk of recurrence. nm23‐H1 targeted treatments may be capable of regulating epithelial‐to‐mesenchymal transition.