This work was possible thanks to a fantastic group of colleagues from @ircm-mtp.bsky.social @ICM_Montpellier @umontpellier.bsky.social
@goteborgsuni @cniostopcancer.bsky.social @CIMA_unav @H12Octubre @nyulangone Thanks a lot to all our great collaborators!! Together we are stronger!!!

This work was possible thanks to a fantastic and complementary group of colleagues from @IRCM_MTP @ICM_Montpellier @umontpellier @goteborgsuni @CNIOStopCancer @CIMA_unav @H12Octubre @nyulangone Thanks a lot to all our great collaborators!! Together we are stronger!!!

As you know, ferroptosis inhibitors are still far from being used in the
clinic, but our findings provide a new way to sensitize cells against them which could
facilitate their clinical translation, at least to treat the leading cause of death by cancer in the
world, i.e., lung.

4. We further dissect the mechanism and uncovered
that FMO4 binds MAT2A, leading to the stabilization of the MAT2A-MAT2B
complex in order to promote the generation of cysteine that in turn regenerates
reduced glutathione to allow GPX4-driven protection against ferroptosis.

2. We demonstrate that FMO is critically required for KRAS-driven lung cancer
generation and maintenance in mice in vivo.
3. We found that FMO4 deletion in lung cancer sensitizes cells against ferroptosis both
in vitro and in vivo, revealing FMO4 as an interesting target in lung cancer.

1. We first found that flavin containing monooxygenase 4
(FMO4) is highly expressed in lung tumors and very low expressed in healthy lung in mouse and lung cancer patients where its expression negatively correlates with patients’ survival.