Event Title

Lipid Starvation Increases Cancer Cell Susceptibility to Ferroptosis

Location

Loosemore Auditorium

Description

PURPOSE: Ferroptosis is an iron-dependent form of programmed cell death that is triggered by the accumulation of lipid reactive oxygen species (ROS). While the entirety of its mechanism is not well understood, this process serves as a major factor in the suppression of tumor growth. The purpose of this study was to examine how the absence of exogenous lipids impacts cancer cell susceptibility to ferroptosis inducers. Subjects: This study was conducted in vitro utilizing the following cancer cell lines: HeLa, MIA PanC1, H1299, PANC1. METHODS: Cells were grown in DMEM culture and then seeded onto a 24-well plate. The growth media was then swapped for +/- lipid containing media containing the ferroptosis inducer RSL3 and cell death dye Sytox Green. Plates were immediately imaged for cell death following the addition of this new media, as well as 24 hours following, and cell death was calculated. RESULTS: HeLa cells showed a concentration dependent increase in cell death of up to 80%. MIA PaCa cells showed a concentration dependent increase in cell death of up to 65%. PANC1 cells showed a concentration dependent increase in cell death of up to 60%. H1299 cells showed a concentration dependent increase in cell death of up to 65%. DISCUSSION AND CONCLUSIONS: The absence of exogenous lipids increased cell susceptibility to ferroptosis. This suggests that exogenous lipids protect cancer cells from ferroptotic cell death.

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Apr 18th, 3:00 PM

Lipid Starvation Increases Cancer Cell Susceptibility to Ferroptosis

Loosemore Auditorium

PURPOSE: Ferroptosis is an iron-dependent form of programmed cell death that is triggered by the accumulation of lipid reactive oxygen species (ROS). While the entirety of its mechanism is not well understood, this process serves as a major factor in the suppression of tumor growth. The purpose of this study was to examine how the absence of exogenous lipids impacts cancer cell susceptibility to ferroptosis inducers. Subjects: This study was conducted in vitro utilizing the following cancer cell lines: HeLa, MIA PanC1, H1299, PANC1. METHODS: Cells were grown in DMEM culture and then seeded onto a 24-well plate. The growth media was then swapped for +/- lipid containing media containing the ferroptosis inducer RSL3 and cell death dye Sytox Green. Plates were immediately imaged for cell death following the addition of this new media, as well as 24 hours following, and cell death was calculated. RESULTS: HeLa cells showed a concentration dependent increase in cell death of up to 80%. MIA PaCa cells showed a concentration dependent increase in cell death of up to 65%. PANC1 cells showed a concentration dependent increase in cell death of up to 60%. H1299 cells showed a concentration dependent increase in cell death of up to 65%. DISCUSSION AND CONCLUSIONS: The absence of exogenous lipids increased cell susceptibility to ferroptosis. This suggests that exogenous lipids protect cancer cells from ferroptotic cell death.