2. Academic Validation
  3. Modulating ovarian cancer progression through FDX1-driven autophagy

Modulating ovarian cancer progression through FDX1-driven autophagy

  • NPJ Precis Oncol. 2025 Jul 8;9(1):230. doi: 10.1038/s41698-025-00994-7.
Chang Liu 1,  Siyu Wang 2,  Jiabao Zhao 1,  Hui Qiu 2,  Hongmei Du 3
Affiliations

Affiliations

  • 1 Department of Pathology, Shengjing Hospital of China Medical University, Shenyang, China.
  • 2 Department of Obstetric and Gynecology, Shengjing Hospital of China Medical University, Shenyang, China.
  • 3 Department of Oncology, Shengjing Hospital of China Medical University, Shenyang, China. dhmcmu@163.com.
PMID: 40629130 DOI: 10.1038/s41698-025-00994-7
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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