A possible regulatory role for nuclear maspin in response to oxidative stress

• Grant number: 21/11576-7
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: March 01, 2022
• End date: December 31, 2022
• Field of knowledge: Biological Sciences - Biochemistry
• Principal Investigator: Nathalie Cella
• Grantee: Juliana Amaral Bichler
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Oxidative stress is known as one of the major factors causing cancer, cardiovascular and neurological diseases, and aging. Within this context, maspin is a tumor suppressor protein that also displays antioxidant properties. It has been reported that cytoplasmic maspin is able to prevent hydrogen peroxide (H2O2)-induced oxidative stress. On the other hand, previous data obtained by our group show that maspin undergoes nuclear translocation upon exposure to H2O2 in the non-tumoral immortalized human keratinocyte cell line (HaCaT), suggesting a role for nuclear maspin in oxidative stress response. We have previously demonstrated that the EGFRPI3K-Akt signaling pathway regulates EGF-induced maspin nuclear accumulation. The same pathway is involved in DNA damage and repair mechanisms triggered by H2O2. Altogether, these data suggest that maspin may integrate EGFR-PI3K-Akt signaling to regulate these nuclear processes. This study aims at investigating maspin nuclear translocation by the EGFR-PI3K-Akt pathway e its putative role in the regulation of the DNA Damage Response (DDR) elicited by H2O2.(AU)