Yujin Dong, Wei Chang, Bei Lu, Yuanyuan Li, Yuanhua Liu
{"title":"mettl5介导的m6A修饰SLC7A11通过抑制铁下垂促进宫颈癌。","authors":"Yujin Dong, Wei Chang, Bei Lu, Yuanyuan Li, Yuanhua Liu","doi":"10.1016/j.biocel.2025.106822","DOIUrl":null,"url":null,"abstract":"<p><p>Ferroptosis could suppress the viability of cervical cancer cells and trigger their death, thereby offering a unique perspective for exploring novel therapeutic approach for cervical cancer. Here, this study tried to explore the role of N<sup>6</sup>-methyladenosine (m<sup>6</sup>A) methyltransferase methyltransferase-like 5 (METTL5) on cervical cancer ferroptosis. Elevated METTL5 functioned as an oncogene in cervical cancer tumorigenesis by inhibiting the ferroptosis. Mechanistically, METTL5 was verified to target SLC7A11 and installed the m<sup>6</sup>A methylation on SLC7A11 mRNA. Moreover, YTHDF3 bound with the m<sup>6</sup>A site of SLC7A11 mRNA to enhance SLC7A11 mRNA stability. Rescue assays confirmed that METTL5/YTHDF3/SLC7A11 axis inhibited the ferroptosis of cervical cancer cells. In vivo, METTL5 silencing repressed the tumor growth of cervical cancer cells, as well as reducing the SLC7A11. In conclusion, these data inspired that METTL5-mediated m<sup>6</sup>A modification of SLC7A11 promoted cervical cancer by inhibiting ferroptosis, providing a novel insight for cervical cancer.</p>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"106822"},"PeriodicalIF":3.4000,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"METTL5-mediated m<sup>6</sup>A modification of SLC7A11 promotes cervical cancer by inhibiting ferroptosis.\",\"authors\":\"Yujin Dong, Wei Chang, Bei Lu, Yuanyuan Li, Yuanhua Liu\",\"doi\":\"10.1016/j.biocel.2025.106822\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Ferroptosis could suppress the viability of cervical cancer cells and trigger their death, thereby offering a unique perspective for exploring novel therapeutic approach for cervical cancer. Here, this study tried to explore the role of N<sup>6</sup>-methyladenosine (m<sup>6</sup>A) methyltransferase methyltransferase-like 5 (METTL5) on cervical cancer ferroptosis. Elevated METTL5 functioned as an oncogene in cervical cancer tumorigenesis by inhibiting the ferroptosis. Mechanistically, METTL5 was verified to target SLC7A11 and installed the m<sup>6</sup>A methylation on SLC7A11 mRNA. Moreover, YTHDF3 bound with the m<sup>6</sup>A site of SLC7A11 mRNA to enhance SLC7A11 mRNA stability. Rescue assays confirmed that METTL5/YTHDF3/SLC7A11 axis inhibited the ferroptosis of cervical cancer cells. In vivo, METTL5 silencing repressed the tumor growth of cervical cancer cells, as well as reducing the SLC7A11. In conclusion, these data inspired that METTL5-mediated m<sup>6</sup>A modification of SLC7A11 promoted cervical cancer by inhibiting ferroptosis, providing a novel insight for cervical cancer.</p>\",\"PeriodicalId\":50335,\"journal\":{\"name\":\"International Journal of Biochemistry & Cell Biology\",\"volume\":\" \",\"pages\":\"106822\"},\"PeriodicalIF\":3.4000,\"publicationDate\":\"2025-06-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Journal of Biochemistry & Cell Biology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1016/j.biocel.2025.106822\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Biochemistry & Cell Biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/j.biocel.2025.106822","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
METTL5-mediated m6A modification of SLC7A11 promotes cervical cancer by inhibiting ferroptosis.
Ferroptosis could suppress the viability of cervical cancer cells and trigger their death, thereby offering a unique perspective for exploring novel therapeutic approach for cervical cancer. Here, this study tried to explore the role of N6-methyladenosine (m6A) methyltransferase methyltransferase-like 5 (METTL5) on cervical cancer ferroptosis. Elevated METTL5 functioned as an oncogene in cervical cancer tumorigenesis by inhibiting the ferroptosis. Mechanistically, METTL5 was verified to target SLC7A11 and installed the m6A methylation on SLC7A11 mRNA. Moreover, YTHDF3 bound with the m6A site of SLC7A11 mRNA to enhance SLC7A11 mRNA stability. Rescue assays confirmed that METTL5/YTHDF3/SLC7A11 axis inhibited the ferroptosis of cervical cancer cells. In vivo, METTL5 silencing repressed the tumor growth of cervical cancer cells, as well as reducing the SLC7A11. In conclusion, these data inspired that METTL5-mediated m6A modification of SLC7A11 promoted cervical cancer by inhibiting ferroptosis, providing a novel insight for cervical cancer.
期刊介绍：
IJBCB publishes original research articles, invited reviews and in-focus articles in all areas of cell and molecular biology and biomedical research.
Topics of interest include, but are not limited to:
-Mechanistic studies of cells, cell organelles, sub-cellular molecular pathways and metabolism
-Novel insights into disease pathogenesis
-Nanotechnology with implication to biological and medical processes
-Genomics and bioinformatics
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