FSP1 in cancer ferroptosis: flowers to brocade or charcoal in snow?

Jingxuan Mao; Tuomas Tammela; Yilong Zou

doi:10.15302/vita.2026.02.0013

Vita > Cutting Edge > DOI: 10.15302/vita.2026.02.0013

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FSP1 in cancer ferroptosis: flowers to brocade or charcoal in snow?

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Lack of safe targets and strategies to induce ferroptosis selectively in cancer cells has precluded targeting ferroptosis as an anti-cancer therapy. Published in Nature, Wu et al. and Palma et al. reveal FSP1 as a more favorable target compared to the conventionally pursued GPX4, showing that FSP1 inhibitors demonstrate a promising therapeutic window in preclinical models of lung cancer and in melanoma lymph node metastasis.

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Ferroptosis is a lipid peroxidation-driven cell death modality. Ample evidence supports that cancer cells may be more vulnerable to ferroptosis induction than normal cells due to their high unsaturated lipidome composition, dysregulated iron surveillance, and high oxidative stress¹. The translation of this concept has remained challenging due to the lack of effective pharmacological agents for induction of ferroptosis selectively in cancer cells in vivo.

The majority of drug development efforts have been directed at targeting glutathione peroxidase-4 (GPX4) — the only cellular enzyme with the capacity for reducing phospholipid hydroperoxides to lipid alcohols and the most potent suppressor of ferroptosis based on genetic experiments. However, targeting GPX4 is hampered by toxicity concerns, which arise from the near-ubiquitous expression of GPX4 in healthy cells and strong requirement of GPX4 for detoxifying lipid peroxidation at basal levels. This concern is further supported by the embryonic lethality of constitutive global knockout of Gpx4 in mice. Furthermore, GPX4 protein levels do not change significantly during tumor progression in models of lung cancer or in several other cancers². Conversely, GPX4 depletion in orthotopic lung cancer allografts promoted tumor growth by inducing DGAT2 expression and accumulation of triacylglycerides³. These results refute the feasibility and efficacy of targeting GPX4 in cancer therapy.

In contrast to equivalent GPX4 protein expression between malignant and healthy cells, Wu et al. reveal that expression of ferroptosis suppressor protein 1 (FSP1, originally named as apoptosis-inducing factor, mitochondrion-associated 2, i.e. AIFM2) becomes induced and correlates with poor prognosis in non-small cell lung cancer (NSCLC)². FSP1-depletion alone is typically insufficient to induce ferroptosis in cultured cancer cells and co-inhibition of GPX4 is a prerequisite for cell death^4,5. However, surprisingly Wu et al. discovered that CRISPR/Cas9-mediated deletion of GPX4 or FSP1 both suppressed lung tumorigenesis², supporting near-equivalent potency in tumor suppression upon loss of function in vivo. These results are notable because Aifm2 knockout mice are viable and fertile, develop normally and exhibit no notable pathologies in adulthood⁶. Collectively, these findings imply a safe on-target toxicity profile for FSP1 inhibitors.

Using recently developed FSP1 inhibitors^5,7,8, Wu et al. and Palma et al. show that pharmacological inhibition of FSP1 alone promotes ferroptosis and significantly suppresses tumor growth in lymph node (LN) niches and in the lung, providing a preclinical proof-of-principle for pharmacological targeting of FSP1 in cancer therapy. Interestingly, one of the FSP1 inhibitors, icFSP1, shows a significant effect only in the autochthonous lung adenocarcinoma (LUAD) model, but not in melanoma LN metastases. icFSP1 is a small molecule that alters FSP1 subcellular localization and augments the effects of ferroptosis inducers⁷. The lack of activity of icFSP1 in LN metastases may be due to the relocation of FSP1 to perinuclear lysosomes and the protein’s acquisition of functional independence from condensate formation. Apart from icFSP1, other FSP1 inhibitors, such as FSEN1 and viFSP1, demonstrate significant anti-tumor effects on LN metastases in vivo. Although the properties and potency of distinct inhibitors in different cancer types warrant further investigation, it is clear from these studies that inhibiting the enzymatic activity of FSP1 represents a promising anti-cancer strategy.

In contrast to the oxygen-rich environment of the lung parenchyma, the LN microenvironment is hypoxic. Palma et al. reveal that hypoxia induces GPX4 protein ubiquitination and proteasomal degradation in melanoma cells⁹, which renders ferroptosis defense in these cells independent of GPX4, instead creating a strong reliance on FSP1 for detoxifying lipid peroxidation. Indeed, FSP1 is upregulated in melanoma cells selected over several passages in vivo for high capacity of LN metastasis. Conversely, the glutathione biosynthesis enzyme GCLC is downregulated in these cells⁹. FSP1 primarily localizes to the perinuclear lysosomes in LN metastatic lines and thus exhibits a different targetability compared with its condensate-associated counterparts⁹. Genetic inactivation of FSP1 potently suppressed melanoma LN metastasis⁹, an effect recapitulated by systemic administration of viFSP1⁹. These findings motivate the further development and evaluation of FSP1 inhibitors in preclinical and clinical studies.

The dependency on FSP1 in vivo may extend to other cancer types and oncogenotypes besides the ones reported by these two studies. In addition to KRAS-mutant cancers, FSP1 is also upregulated in EGFR-mutant lung cancers². Moreover, FSP1 is required for the survival of drug-tolerant persister cells that have survived GPX4 inhibition in multiple cancer lineages¹⁰. Drivers of FSP1 upregulation remain unclear, however activation of the master cellular antioxidant response via NRF2 downstream of oncogenic KRAS signaling is one plausible possibility^11,12. Curiously, these studies find that GPX4 — also an NRF2 target — is not induced by the same program in these cancer contexts.

The works of Wu et al. and Palma et al. raise several mechanistically important future questions: First, cell death induced by FSP1 deletion appears primarily cell-intrinsic, without dramatic alterations in the major immune cell populations². This is notable given that non-cancer cell autonomous modulation of microenvironmental cells is a long-held hypothesis for lytic cell death by ferroptosis. As such, the immunogenic effects of FSP1-suppression await further characterization in diverse contexts. FSP1 activity is critical for the survival of immunosuppressive regulatory T (T_reg) cells, but not the antigen-specific CD8⁺ cytotoxic T cells in the tumor microenvironment¹³, suggesting an additional therapeutically favorable, cancer cell-extrinsic effect of FSP1 inhibitors on anti-tumor immunity. Second, the mechanism regulating cell type-specific subcellular localization of FSP1, including to the plasma membrane, lysosomes, mitochondria, lipid droplets, and condensates etc., remains unclear^7,9,14,15. Third, the generalizability of hypoxia-regulated GPX4 protein stability awaits to be further assessed⁹. It is worth noting that these studies were performed under the scenario of no bioavailable GPX4 inhibitor could be used for in vivo studies, and thus the therapeutic window for using GPX4 inhibitors as single agents for tumor suppression remain elusive rather than disproved; and the comparative advantage of either inhibitor is unclear.

The clinical development of FSP1-directed anti-cancer therapies would be greatly aided by a biomarker, such as FSP1 protein expression level, to predict sensitivity to FSP1 inhibitors. Pharmacological strategies including targeted drug delivery, as well as targeted protein degradation, may further expand the therapeutic window. Additionally, ongoing efforts in the development of selective and bioavailable GPX4 inhibitors may enhance ferroptosis induction efficacy by permitting combined use with FSP1 inhibitors.

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[3]	Wang, P. et al. Protein Cell https://doi.org/10.1093/procel/pwaf101 (2025).

[4]	Bersuker, K. et al. Nature 575, 688–692 (2019).

[5]	Doll, S. et al. Nature 575, 693–698 (2019).

[6]	Mei, J., Webb, S., Zhang, B. & Shu, H.B. Oncogene 25, 849–856 (2006).

[7]	Nakamura, T. et al. Nature 619, 371–377 (2023).

[8]	Hendricks, J.M. et al. Cell Chem. Biol. 30, 1090–1103.e7 (2023).

[9]	Palma, M. et al. Nature 649, 477–486 (2026).

[10]	Higuchi, M. et al. Sci. Adv. 12, eaea8771 (2026).

[11]	Müller, F. et al. Cell Death Differ. 30, 442–456 (2023).

[12]	Ma, S. et al. Cell Rep. 44, 116234 (2025).

[13]	Castillo, J.G. et al. Sci. Adv. 12, eaea3703 (2026).

[14]	Yang, J.S. et al. Cell 188, 2569–2585.e20 (2025).

[15]	Lange, M. et al. Nat. Cell Biol. 27, 1902–1913 (2025).

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Mao, J., Tammela, T., Zou, Y. FSP1 in cancer ferroptosis: flowers to brocade or charcoal in snow? Vita https://doi.org/10.15302/vita.2026.02.0013 ()

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