ArticleNPJ precision oncology2025
Modulating ovarian cancer progression through FDX1-driven autophagy.
Article in NPJ precision oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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
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Who cites it
5 citing papers in PubMed.
- Metabolic cell death: ferroptosis, cuproptosis, and disulfidptosis as a unified framework for targeting metabolic vulnerabilities in disease.Apoptosis : an international journal on programmed cell death · 2026Review
- Role of Ferredoxin 1Cancer pathogenesis and therapy · 2026Review
- Advancing the frontiers of ovarian cancer therapy: a comprehensive synthesis of emerging cell death paradigms.Oncology reviews · 2026Review
- Regulated cell death in ovarian cancer: molecular mechanisms and therapeutic targets.Frontiers in cell and developmental biology · 2026Review
- Inhibition of the Sp1/CTR1 axis attenuates cuproptosis and alleviates axonal injury following intracerebral hemorrhage.Frontiers in molecular biosciences · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferredoxin 1 (FDX1) emerges as a crucial regulator of autophagy and copper metabolism in ovarian cancer (OC), as revealed by this investigation. Predominantly localized to the cytoplasm and mitochondria, FDX1 coordinates autophagic activity by modulating the AMPK and mTOR signaling pathways. Its role extends to preserving mitochondrial integrity and facilitating sulfation of DLAT/DLST, ensuring effective autophagic flux. Knockdown of FDX1 disrupts these processes, exacerbating mitochondrial dysfunction. In vivo studies further demonstrate that overexpressing FDX1, combined with Compound C treatment, markedly inhibits tumor growth and Ki67 expression. These results position FDX1 as a promising target for therapeutic strategies aimed at exploiting autophagy to hinder OC progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.