ITM1 and C1orf24, cell sublocation, identification of genes that are modulated by ectopic expression and characterization

• Grant number: 12/02325-1
• Support Opportunities: Scholarships in Brazil - Doctorate (Direct)
• Start date: May 01, 2012
• End date: April 30, 2017
• Field of knowledge: Health Sciences - Medicine
• Principal Investigator: Janete Maria Cerutti
• Grantee: Bruno Heidi Nakano Nozima
• Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

Previous studies from our group demonstrated that STT3A (Integral TransMembrane protein 1), also named STT3A, and C1orf24 (Chromosome 1 Open Reading Frame 24), also named FAM129A, are over expressed in thyroid carcinomas. Further validation analysis using imunohistochemistry analysis, demonstrated that STT3A and C1orf 24 can distinguish begin from malignant thyroid tumors with high sensibility and specificity (100% and 85% for ITM1; 97% and 90% for C1orf24, respectively). These findings suggested that both genes are important preoperative diagnostic markers for thyroid nodules. Despite of their relevance as preoperative diagnosis markers, little is known about their role in tumor's pathogenesis and/or progression. This project aims to investigate the sublocation of these proteins in normal and pathological processes of thyroid. Then, we´ll identify genes potentially modulated by ectopic expression of ITM1 and C1orf24. We´ll first clone the cDNA of the STT3A and C1orf24 in pBudCE4.1. To indentify which in vitro model could be best used to ectopically express STT3A, several cell lines available will be evaluated for the expression of STT3A and C1orf24 at both mRNA and protein levels. Subsequently, we´ll permanently transfect the vector expressing cDNA of STT3A or C1orf24 and control vector into the appropiate cell line model by magnet assisted transfection. By PCR Array, genes modulated by ITM1 and C1orf24 will be identified and then validated in frozen tissues. Finally, we will analyze the effects of the ectopic expression of ITM1 and C1orf in mammals cells. (AU)