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Eur Arch Otorhinolaryngol. 2018 Dec;275(12):3039-3047. doi: 10.1007/s00405-018-5182-2. Epub 2018 Oct 26.

Abnormal activation of the Akt signaling pathway in adenoid cystic carcinoma.

Author information

1
Cell Culture Laboratory, School of Dentistry, Federal University of Pará (UFPA), Belém, PA, Brazil.
2
Department of Oral and Maxillofacial Surgery, School of Dentistry, University Center of Pará-CESUPA, Travessa 9 de Janeiro, 827, Belem, PA, 66013 090, Brazil. andre.ribeiro.13@ucl.ac.uk.
3
MPCO Graduate Program, School of Dentistry, University Centre of Pará-CESUPA, Belém, PA, Brazil. andre.ribeiro.13@ucl.ac.uk.
4
Department of Pathology, Ophir Loyola Hospital, Belém, Brazil.

Abstract

PURPOSE:

Adenoid cystic carcinoma (ACC) is an intriguing lesion because it shows a slow growth in the beginning, but a late poor prognosis due to perineural invasion, metastasis and recurrence. This study aimed to investigate whether Akt signaling would be deregulated in adenoid cystic carcinoma and its consequence in the expression of associated proteins.

METHODS:

The expression of the Akt, p-Akt, NFκB, β-catenin, cyclin D1 and COX-2 was assessed by immunohistochemistry in 10 cases of ACC, 17 cases of pleomorphic adenoma (PA), and 7 cases of normal salivary gland (NSG).

RESULTS:

p-Akt was overexpressed in ACC when compared to NSG. NFκB, β-catenin, and COX-2 were overexpressed in ACC and PA when compared to NSG. Most proteins were slightly higher expressed in ACC than in PA, but they never reached significance. p-Akt expression positively correlated with NFκB, β-catenin, cyclin D1 and COX-2 in ACC and PA, while this correlation trended to be negative in for these proteins (except for NFκB) in NSG using Person's correlation analysis, but without reaching significance.

CONCLUSIONS:

Our results indicate an abnormal activation of Akt signaling pathway, which can be an important regulator of tumor biology in ACC. Activated Akt correlated with the expression of NFκB, β-catenin and COX-2, which can potentially influence cell survival in ACC.

KEYWORDS:

Adenoid cystic carcinoma; Akt; NFκB; Pleomorphic adenoma; Salivary gland tumors

PMID:
30367261
DOI:
10.1007/s00405-018-5182-2

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