Cortactin and phosphorylated cortactin tyr466 expression in temporal bone carcinoma

Publication date: Available online 19 January 2017
Source:American Journal of Otolaryngology
Author(s): Gino Marioni, Elisabetta Zanoletti, Antonio Mazzoni, Andrea Gianatti, Elisa Valentini, Laura Girasoli, Martina Guariento, Luciano Giacomelli, Alessandro Martini, Stella Blandamura
PurposeCortactin is a multidomain protein engaged in several cellular mechanisms involving actin assembly and cytoskeletal arrangement. Cortactin overexpression in several malignancies has been associated with increased cell migration, invasion, and metastatic potential. Cortactin needs to be activated by tyrosine or serine/threonine phosphorylation. The role of cortactin and phosphorylated cortactin (residue tyr⁴⁶⁶) was investigated in temporal bone squamous cell carcinoma (TBSCC).Materials and methodsImmunohistochemical expression of cortactin and phosphorylated cortactin (residue tyr⁴⁶⁶) was assessed in 27 consecutively-operated TBSCCs.ResultsSeveral clinicopathological variables correlated with recurrence (pT stage, dura mater involvement), and disease-free survival (DFS) (cT stage, pT stage, pN status, dura mater involvement). Twenty-three of 24 immunohistochemically evaluable TBSCCs were cortactin-positive. Median cortactin expression was 75.0%. Cortactin reaction in the cytoplasm was more intense in carcinoma cells than in normal adjacent tissue. Recurrence and DFS rates did not correlate with cortactin and phosphorylated cortactin (residue tyr⁴⁶⁶) expression in TBSCC specimens.ConclusionsCortactin upregulation in TBSCC supports the conviction that inhibiting cortactin functions could have selective effects on this malignancy. Multi-institutional studies should further investigate the role of cortactin and phosphorylated cortactin in TBSCC, and their potential clinical application in integrated treatment modalities.



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