Investigation of Methionine Sulfoxide Reductase A in Germ Cell Tumors

• Grant number: 24/02992-5
• Support Opportunities: Scholarships abroad - Research Internship - Master's degree
• Effective date (Start): August 15, 2024
• Effective date (End): February 14, 2025
• Field of knowledge: Biological Sciences - Genetics - Human and Medical Genetics
• Principal Investigator: Mariana Tomazini Pinto
• Grantee: Lenilson Silva
• Supervisor: Shailaja Allani
• Host Institution: Hospital do Câncer de Barretos. Fundação Pio XII (FP). Barretos , SP, Brazil
• Research place: Florida Atlantic University, Jupiter Campus, United States
• Associated to the scholarship: 23/07073-5 - Epithelial-mesenchymal transition: implications in pediatric patients with germ cell tumors, BP.MS

Abstract

Germ cell tumors (GCTs) are complex neoplasms with varying histological subtypes and clinical characteristics that present significant treatment challenges, particularly in pediatric cases and when exhibiting resistance to standard therapies like cisplatin. This project aims to investigate the role of Methionine Sulfoxide Reductase A (MSRA) in GCT pathogenesis, focusing on its expression levels in GCT cell lines and its correlation with tumor proliferation rates and metastatic potential. MSRA enzymatic activity and protein expression will be evaluated in NTERA-2 parental, NTERA-2 cisplatin-resistant and 1777N GCT cell lines using enzymatic assay and Western blotting, respectively. Additionally, functional assays, including migration and proliferation tests, will be conducted to correlate MSRA levels with the aggressive behaviors of GCT cell lines at The Center for Molecular Biology and Biotechnology at Florida Atlantic University. This study addresses the need for new therapeutic targets in metastatic and cisplatin-resistant GCTs. Given that 15-20% of metastatic GCT patients lack curative options after relapse, exploring MSRA's role opens potential avenues for treatment innovation. The project's findings could significantly contribute to understanding GCT pathogenesis and overcoming current therapeutic limitations.