Role of the microRna-106B and C1orf24 gene in the cell migration process of the human thyroid tumors

• Grant number: 15/04164-3
• Support Opportunities: Regular Research Grants
• Start date: December 01, 2015
• End date: May 31, 2018
• Field of knowledge: Biological Sciences - Genetics - Human and Medical Genetics
• Principal Investigator: Gianna Maria Griz Carvalheira
• Grantee: Gianna Maria Griz Carvalheira
• Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil
• Associated researchers: Janete Maria Cerutti

Abstract

Previous studies from our group, using SAGE (Serial Analysis of Gene Expression), showed the C1orf24 (Chromosome 1 Open Reading Frame 24) is highly expressed in follicular thyroid carcinomas. Further validation by immunohistochemistry demonstrated that C1orf24 in one of the biomarkers that can help to distinguish benign from malign lesions, suggesting its application in preoperative diagnosis of thyroid nodules. As result from our previous project, supported by FAPESP 2012/02902-9, we showed that the C1orf24 expression in thyroid carcinomas is, in part, regulated by microRNA-106b. Next, we demonstrated that ectopic expression of miR-106b in a thyroid carcinoma cell line (WRO) not only direct inhibited C1orf24 expression but also significantly inhibited cell migration. Therefore, the main goal of this project is to further clarify if the correlation between C1orf24 and miR-106b expression play an important role in migration process in thyroid carcinomas and to identify the signaling pathway potentially associated in this process. Once protein networks are identified, we will validate their expressions in metastatic and non-metastatic thyroid carcinomas and correlate their expression with C1orf24 and miR-106b expression. Whether the genes involved in cell migration pathways present expression alteration in thyroid lesions, we will perform in vitro assays: re-expression of C1orf24, by permanent transfection, and silencing C1orf24 expression, by miR-106b. The main objective of these assays is to verify if these genes are modulated by C1orf24 as well as to understand their effects in the cell migration. Then, we plan to comprehend the role of C1orf24 and miR-106b in the cell migration during the human thyroid carcinogenesis process. (AU)