Elevated GPx4 and FSP1 expression in MG63 cells: Exploring potential links to drug resistance and ferroptosis

Osteosarcoma (OS) treatments currently rely on a combination of surgery and chemotherapy. However, the development of drug resistance remains a major obstacle, significantly impacting the five-year survival rate of OS patients. Addressing this issue requires new therapeutic approaches. Ferroptosis, a type of regulated cell death driven by oxidative stress, has emerged as a potential mechanism for cancer treatment. Ferroptosis is distinct from other forms of cell death and has been explored in various cancers, but its role in OS remains under investigation. We hypothesized that the antioxidant enzymes GPx4 and FSP1 are expressed at significantly higher levels in OS cells, particularly in MG63 cells, compared to healthy osteoblasts. This elevated expression suggests a potential role in inhibiting ferroptosis. To explore this, we investigated the differential expression of GPx4 and FSP1 in MG63 cells and healthy osteoblasts to understand their relationship to ferroptosis inhibition. Our results support this hypothesis, showing that higher levels of GPx4 and FSP1 in MG63 cells correlate with inhibition of the ferroptosis pathway. This suggests that the accumulation of these proteins plays a role in blocking ferroptosis, potentially contributing to drug resistance in OS. These findings open the door to new therapeutic strategies aimed at overcoming drug resistance by targeting the pathways that regulate ferroptosis. By manipulating these mechanisms, we may be able to enhance the effectiveness of chemotherapy and improve patient outcomes.