ArticleOncogene2022
METTL3 potentiates progression of cervical cancer by suppressing ER stress via regulating m6A modification of TXNDC5 mRNA.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- WTAP-Mediated m6A Modification of TXNDC5 mRNA Promotes Cervical Carcinogenesis.The Kaohsiung journal of medical sciences · 2026Article
- The Role of NMedComm · 2026Review
- Unravelling Multilayered RNA Modification Networks in Female Reproduction and Obstetric/Gynaecologic Disorders.Biomolecules · 2026Review
- Filgotinib inhibits METTL3-mediated mNPJ precision oncology · 2026Article
- Loss of METTL14 in dopaminergic neurons disrupts ER homeostasis via m6A-dependent regulation of Atp2a3 mRNA: Implications for Parkinson's Disease.NPJ Parkinson's disease · 2026Article
- m6A modification and its clinical applications in gynaecological cancer.Apoptosis : an international journal on programmed cell death · 2026Review
- ALKBH5-mediated m6A demethylation of TXNDC5 drives malignant progression in gastric cancer.Epigenomics · 2026Article
- Uncomplexed-TSC1 deploys novel mTORC1-independent pathway to exacerbate the liver glycogen storage in TSC.Cell death & disease · 2025Article
- Epigenetic Biomarkers for Cervical Cancer Progression: A Scoping Review.International journal of molecular sciences · 2025Article
- N6-methyladenosine in cervical carcinogenesis: Mechanistic insights and therapeutic perspectives (Review).Oncology letters · 2025Review
- Article
- Advances in understanding the mechanisms of the human papillomavirus oncoproteins.Biochemical Society transactions · 2025Review
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- METTL3-dependent DLG2 inhibits the malignant progression of cervical cancer by inactivating the Hippo/YAP signaling.Hereditas · 2025Article
- N6-methyladenosine RNA modification regulates the transcription of SLC7A11 through KDM6B and GATA3 to modulate ferroptosis.Journal of biomedical science · 2025Article
- Genetic dysregulation of EP300 in cancers in light of cancer epigenome control - targeting of p300-proficient and -deficient cancers.Molecular therapy. Oncology · 2024Review
- Epitranscriptomics and cervical cancer: the emerging role of mExpert reviews in molecular medicine · 2024Review
- METTL protein family: focusing on the occurrence, progression and treatment of cancer.Biomarker research · 2024Review
- Unraveling the molecular complexity: Wtap/Ythdf1 and Lcn2 in novel traumatic brain injury secondary injury mechanisms.Cell biology and toxicology · 2024Article
- NCellular and molecular life sciences : CMLS · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N6-methyladenosine (m6A) is the most abundant chemical modification on mRNA and plays significant roles in many bioprocesses. However, the functions of m6A on cervical cancer (CC) tumorigenesis remain unclear. Here we found methyltransferase-like 3 (METTL3), a core member of the m6A methyltransferase family, was greatly upregulated as an independent prognostic factor in CC. Mechanistically, the transcription factor ETS1 recruited P300 and WDR5 which separately mediated H3K27ac and H3K4me3 histone modification in the promoter of METTL3 and induced METTL3 transcription activation. Furthermore, we identified TXNDC5 as a target of METTL3-mediated m6A modification through MeRIP-seq, and revealed that METTL3-mediated TXNDC5 expression relied on the m6A reader-dependent manner. Functionally, we verified that METTL3 promoted proliferation and metastasis of CC cells by regulating of TXNDC5 expression through in vitro and in vivo experiments. In addition, our study verified the effect of METTL3/TXNDC5 axis on ER stress. Taken together, METTL3 facilitates the malignant progression of CC, suggesting that METTL3 might be a potential prognostic biomarker and therapeutic target for CC.
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