Presenter: Pari Samir Khandhar
Faculty Sponsor: Rachid Skouta
School: UMass Amherst
Research Area: Biochemistry and Molecular Biology
ABSTRACT
Ferroptosis is a form of non-apoptotic cell death regulated by genetic and biochemical pathways. It occurs when the enzyme responsible for preventing lipid peroxidation, glutathione peroxidase 4 (GPX4), is inhibited, leading to accumulation of lipid hydroperoxides and cell death. Cancer cells, which often contain high levels of iron, are particularly sensitive to ferroptosis due to iron-catalyzed amplification of lipid peroxidation. Chemical inducers of ferroptosis can trigger this pathway by promoting lipid peroxidation and overwhelming the cell’s antioxidant defenses. In these studies, a novel ferroptosis-activating compound was tested in human cancer cell lines. The compound induced dose-dependent cell death characterized by accumulation of lipid reactive oxygen species and was suppressed by known ferroptosis inhibitors, confirming engagement of the pathway. These findings highlight ferroptosis as a chemically inducible form of cell death and underscore its potential as a therapeutic target for diseases where apoptosis and traditional cell-death mechanisms are ineffective. This work supports the continued development of ferroptosis-targeted strategies for cancer therapy and other disease contexts.
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