Different isoforms of GSK3 protein expression in adenoid cystic Carcinoma of salivary gland

• Grant number: 14/01255-5
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Effective date (Start): April 01, 2014
• Effective date (End): March 31, 2015
• Field of knowledge: Health Sciences - Dentistry
• Principal Investigator: Yasmin Rodarte Carvalho
• Grantee: Bruna Emi Takamura
• Host Institution: Instituto de Ciência e Tecnologia (ICT). Universidade Estadual Paulista (UNESP). Campus de São José dos Campos. São José dos Campos , SP, Brazil

Abstract

The Phosphatydilinositol 3-kinase (PI3K/Akt) pathway is altered in many human cancers and it is widely studied in many glandular tumors as, breast and prostate carcinomas. In relation to salivary gland neoplasia, previous studies have been demonstrated dysregulation of PI3K signaling as, Akt overexpression, in adenoid cystic carcinoma. Glycogen Synthase Kinase 3 (GSK3) is a well-established downstream component of PI3K signaling pathway but is also a key enzyme in negatively regulating the canonical Wnt/²-catenical signaling pathway. Studies argue that Akt-mediated inhibition leads to ²-catenin accumulation and, consequently, increases the transcription of genes related to cell cycle progression. In the present study we aim to investigate the GSK3 isoform protein expression in adenoid cystic carcinoma of salivary gland compared with normal salivary gland through immunohistochemical assay for GSK3± and GSK3² proteins in tissue microarray slides. (AU)