ArticleJournal of ovarian research2025
LncRNA AC040169.1 is regulated by m6A modification and suppresses ferroptosis via SLC7A11 to promote ovarian cancer progression.
Article in Journal of ovarian research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- The progress of mitochondrial function and transfer in stem cell regulation and therapy.Journal of physiology and biochemistry · 2026Review
- Advances in ferroptosis research in ovarian cancer: molecular mechanisms and therapeutic perspectives.American journal of cancer research · 2026Review
- RNA m6A modification-regulated ferroptosis in cancer: mechanism and therapeutic potential.Frontiers in cell and developmental biology · 2026Review
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5 authors.
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Abstract
backgroundOvarian cancer (OC) is a common malignant tumour of the female reproductive system. Long noncoding RNAs (lncRNAs) and m6A modifications play important regulatory roles in tumour cells. Ferroptosis is closely related to tumour development, but the function and molecular mechanism of lncRNAs in ferroptosis are still unclear.
methodsThe expression of AC040169.1 was detected in OC cells and tissues. The molecular mechanism by which METTL14 and YTHDC2 up-regulate the level of AC040169.1 with m6A modification is investigated. Furthermore, the biological functions of AC040169.1 and ferroptosis in OC cells were investigated in vivo and in vitro.
resultsIn the present study, the expression of AC040169.1, a lncRNA, was first shown to be upregulated in OC. Mechanistically, low levels of METTL14 reduced the m6A modification of AC040169.1 and increased the stability of AC040169.1, mainly via the decreased recognition and binding abilities of the “reader” YTHDC2. The subsequently enhanced downstream target SLC7A11 promoted the malignancy and inhibited ferroptosis of OC cells.
conclusionsour findings reveal that m6A modification upregulates lncRNA AC040169.1 expression, which inhibits ferroptosis and promotes OC progression. These findings provide both theoretical and experimental evidence supporting lncRNA AC040169.1 as an epigenetic biomarker and potential therapeutic target for OC.
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