ArticleCell death & disease2025
piR-26441 inhibits mitochondrial oxidative phosphorylation and tumorigenesis in ovarian cancer through m6A modification by interacting with YTHDC1.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- The Role of NMedComm · 2026Review
- Unravelling Multilayered RNA Modification Networks in Female Reproduction and Obstetric/Gynaecologic Disorders.Biomolecules · 2026Review
- piR-1170 drives brain metastasis and immune evasion via WTAP-mediated m6A methylation reprogramming in triple-negative breast cancer.Molecular cancer · 2026Article
- Pharmacologic reversal of advanced Alzheimer's disease in mice and identification of potential therapeutic nodes in human brain.Cell reports. Medicine · 2026Article
- Characterization of mEuropean journal of medical research · 2025Article
- The mMolecular biomedicine · 2025Review
- Reciprocal regulation between m6 A modifications and non-coding RNAs: emerging roles in cancer therapeutic resistance.Discover oncology · 2025Review
- The epitranscriptome meets non-coding RNA: m6A-mediated regulation in oncogenesis and therapy.Frontiers in cell and developmental biology · 2025Review
- Cracking the code: how piRNA pathway shapes spermatogenesis and combats male infertility.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
Ovarian cancer (OC) is a heterogeneous cancer. In contrast to other tumor cells, which rely primarily on aerobic glycolysis (Warburg effect) as their energy source, oxidative phosphorylation (OXPHOS) is also one of its major metabolic modes. Piwi-interacting RNAs (piRNAs) play a regulatory function in various biological processes in tumor cells. However, the role and mechanisms of piRNAs in OC and mitochondrial OXPHOS remain to be elucidated. Here, we found that piR-26441 was aberrantly downregulated in OC, and its overexpression suppressed the malignant features of OC cells and tumor growth in a xenograft model. Moreover, overexpression of piR-26441 significantly reduced mitochondrial OXPHOS levels in OC cells. Furthermore, piR-26441 directly binds to and upregulates the expression of YTHDC1 in OC cells. piR-26441 also increased m6A levels, thereby interacting with YTHDC1 to destabilize the mRNA of TSFM. The resultant TSFM loss reduced mitochondrial complex I activity and mitochondrial OXPHOS, leading to mitochondrial dysfunction in OC cells, increased reactive oxygen species levels, and thus, DNA damage and apoptosis in OC cells, thereby inhibiting OC progression. Additionally, ago-piR-26441 suppressed tumor growth and mitochondrial metabolism in the patient-derived organoid model. Altogether, piR-26441 could inhibit OC cell growth via the YTHDC1/TSFM signaling axis, underscoring its significant importance in the context of OC, as well as offering potential as a therapeutic target.
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