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Background <p>Ovarian 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.</p> Methods <p>The 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 <i>vivo</i> and in <i>vitro</i>.</p> Results <p>In 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.</p> Conclusions <p>our 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.</p>

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LncRNA AC040169.1 is regulated by m6A modification and suppresses ferroptosis via SLC7A11 to promote ovarian cancer progression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月28日

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  • Huilin Yang,
  • Ying Dong,
  • Rongji Li,
  • Longyan Zhu,
  • Lihua Yang

摘要

Background

Ovarian 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.

Methods

The 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.

Results

In 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.

Conclusions

our 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.