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Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
Modulating ovarian cancer progression through FDX1-driven autophagy
Chang Liu1, Siyu Wang2, Jiabao Zhao1
1Department of Pathology, Shengjing Hospital of China Medical University, Shenyang, China.
None:
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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