ArticleThe Journal of biological chemistry2026
The iron-sulfur cluster assembly factor FDX2 is required for tumor initiation but not for growth of established tumors in transplantation models.
Article in The Journal of biological chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Iron Metabolism in the Colorectal Tumor Microenvironment: From Preneoplastic Lesions to Cancer Progression.International journal of molecular sciences · 2026Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iron-sulfur (Fe-S) clusters bind to Fe-S proteins and are required for their function and/or structural stability. Recent work reveals an essential role for Fe-S cluster biosynthesis in cancer cell proliferation in vitro, but how Fe-S cluster metabolism contributes to tumor activity in vivo is unclear. Here we report analysis suggesting a stage-specific requirement for FDX2, a critical component of the Fe-S cluster assembly complex, in cancer progression. Using inducible loss-of-function transplant models of a human ovarian cancer line, we show that FDX2 is required for tumor initiation and metastasis but not for growth of established tumors in mice. We report global upregulation of Fe-S proteins under low oxygen conditions and concomitant attenuation of FDX2 loss-mediated disruption of many Fe-S proteins, enabling FDX2-independent proliferation. Our findings highlight a differential requirement of Fe-S cluster biosynthesis for tumor metastasis versus growth and low oxygen-mediated mitigation of Fe-S protein loss promoted by FDX2 deficiency.
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