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         headline:NFS1 undergoes positive selection in lung tumours and protects cells from ferroptosis
         description:Cancers growing in high-oxygen environments, such as lung adenocarcinomas, select for the iron–sulfur cluster synthesizing enzyme NFS1 to support malignant proliferation and to protect from oxidative damage. Cancer cells often select environment-specific adaptations in order to grow in different contexts. The authors show that tumours growing in high oxygen settings, such as lung cancers or metastasis, usually show elevated NFS1 signalling. NFS1 maintains the iron–sulfur clusters in proteins that are essential for protecting them from oxidative damage. Inactivating NFS1 or iron–sulfur clusters can trigger ferroptosis, a non-apoptotic form of cell death, in cancer cells. Environmental nutrient levels impact cancer cell metabolism, resulting in context-dependent gene essentiality1,2. Here, using loss-of-function screening based on RNA interference, we show that environmental oxygen levels are a major driver of differential essentiality between in vitro model systems and in vivo tumours. Above the 3–8% oxygen concentration typical of most tissues, we find that cancer cells depend on high levels of the iron–sulfur cluster biosynthetic enzyme NFS1. Mammary or subcutaneous tumours grow despite suppression of NFS1, whereas metastatic or primary lung tumours do not. Consistent with a role in surviving the high oxygen environment of incipient lung tumours, NFS1 lies in a region of genomic amplification present in lung adenocarcinoma and is most highly expressed in well-differentiated adenocarcinomas. NFS1 activity is particularly important for maintaining the iron–sulfur co-factors present in multiple cell-essential proteins upon exposure to oxygen compared to other forms of oxidative damage. Furthermore, insufficient iron–sulfur cluster maintenance robustly activates the iron-starvation response and, in combination with inhibition of glutathione biosynthesis, triggers ferroptosis, a non-apoptotic form of cell death. Suppression of NFS1 cooperates with inhibition of cysteine transport to trigger ferroptosis in vitro and slow tumour growth. Therefore, lung adenocarcinomas select for expression of a pathway that confers resistance to high oxygen tension and protects cells from undergoing ferroptosis in response to oxidative damage.
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      headline:NFS1 undergoes positive selection in lung tumours and protects cells from ferroptosis
      description:Cancers growing in high-oxygen environments, such as lung adenocarcinomas, select for the iron–sulfur cluster synthesizing enzyme NFS1 to support malignant proliferation and to protect from oxidative damage. Cancer cells often select environment-specific adaptations in order to grow in different contexts. The authors show that tumours growing in high oxygen settings, such as lung cancers or metastasis, usually show elevated NFS1 signalling. NFS1 maintains the iron–sulfur clusters in proteins that are essential for protecting them from oxidative damage. Inactivating NFS1 or iron–sulfur clusters can trigger ferroptosis, a non-apoptotic form of cell death, in cancer cells. Environmental nutrient levels impact cancer cell metabolism, resulting in context-dependent gene essentiality1,2. Here, using loss-of-function screening based on RNA interference, we show that environmental oxygen levels are a major driver of differential essentiality between in vitro model systems and in vivo tumours. Above the 3–8% oxygen concentration typical of most tissues, we find that cancer cells depend on high levels of the iron–sulfur cluster biosynthetic enzyme NFS1. Mammary or subcutaneous tumours grow despite suppression of NFS1, whereas metastatic or primary lung tumours do not. Consistent with a role in surviving the high oxygen environment of incipient lung tumours, NFS1 lies in a region of genomic amplification present in lung adenocarcinoma and is most highly expressed in well-differentiated adenocarcinomas. NFS1 activity is particularly important for maintaining the iron–sulfur co-factors present in multiple cell-essential proteins upon exposure to oxygen compared to other forms of oxidative damage. Furthermore, insufficient iron–sulfur cluster maintenance robustly activates the iron-starvation response and, in combination with inhibition of glutathione biosynthesis, triggers ferroptosis, a non-apoptotic form of cell death. Suppression of NFS1 cooperates with inhibition of cysteine transport to trigger ferroptosis in vitro and slow tumour growth. Therefore, lung adenocarcinomas select for expression of a pathway that confers resistance to high oxygen tension and protects cells from undergoing ferroptosis in response to oxidative damage.
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