# Ferroptosis in the U87MG Human Glioblastoma Cell Line Induces Damage Associated Molecular Phenotypes

## TL;DR

Inducing ferroptosis in glioblastoma cells may transform them from immune cold to immune hot, making them more responsive to immunotherapy.

## Contribution

Demonstrates that ferroptosis in U87MG glioblastoma cells induces DAMPS, suggesting a novel therapeutic strategy.

## Key findings

- Ferroptosis induced by Erastin and OGM leads to DAMPS release in U87MG cells.
- This suggests ferroptosis could convert glioblastomas to immune hot cancers.
- The findings highlight ferroptosis as a potential mechanism for glioblastoma immunotherapy.

## Abstract

Glioblastomas are known as “immune cold” cancers with little induction of damage-associated molecular phenotypes (DAMPS). We previously described the induction of ferroptosis in glioblastoma cells using the small molecule, OGM, a specific inhibitor of GPR68. The ferroptotic cell death pathway has been reported to induce the release of DAMPS. Here, we show that induction of ferroptosis through both Erastin and OGM results in DAMPS in U87MG cells. This suggests that ferroptosis in human glioblastomas may be able to convert them to an “immune hot” cancer, increasing their susceptibility to immunotherapy. These findings highlight the immunogenic potential of causing ferroptosis in glioblastoma as a therapeutic mechanism of action.