ArticleMolecular cancer2019
METTL3 promote tumor proliferation of bladder cancer by accelerating pri-miR221/222 maturation in m6A-dependent manner.
Article in Molecular cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 454 papers, 1 of them a synthesis that pooled it.
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Who cites it
454 citing papers in PubMed, 1 synthesis or guideline pooled it, 739 citations in OpenAlex.
- The relationship between the network of non-coding RNAs-molecular targets and N6-methyladenosine modification in tumors of urinary system.Cell death & disease · 2024Pooled it
- Exosomal delivery of METTL3 promotes M1 macrophage polarization by inducing miR-155-5p maturation via m6A modification.Annals of medicine · 2026Article
- m6A-modified circCD2AP suppressed ferroptosis in bladder cancer by upregulating FOXC1 to promote PARK7 transcriptional activity.Chinese medical journal · 2026Article
- Regulatory roles of N6-methyladenosine methylation factors in melanoma invasion and metastasis (Review).Oncology letters · 2026Review
- Characterization of Circ_0048766: an oncogenic circular rna promoting triple-negative breast cancer progression via the miR-329-3p/CXCR4 axis and regulated by METTL3.Cancer cell international · 2026Article
- mBiomolecules · 2026Review
- RNA methylation in cell death: mechanisms and clinical applications.Molecular cancer · 2026Review
- Review
- The impact of m6A modified cargo conveyed by exosomes on the tumor microenvironment.Discover oncology · 2026Review
- Identification of METTL3 and PRMT5 as an oncogenic pair for the prognosis and therapeutic targets of colorectal cancer subtype.Clinical epigenetics · 2026Article
- RBM15/IGF2BP2-PTPRH m6A regulatory axis in non-small cell lung cancer.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- The mechanism by which methylase METTL3 affects intramuscular fat deposition.Poultry science · 2026Article
- KIAA1429 promotes clear cell renal cell carcinoma progression by regulating MYC mRNA stability.iScience · 2026Article
- N6-methyladenosine-modified miR-873 promotes receptor-interacting protein kinase 3-mediated necroptosis after intracerebral hemorrhage in mice and HT22 cells.Neuroreport · 2026Article
- RBM15 drives bladder cancer progression through YTHDF2-dependent m6A-mediated regulation of ZO2.Journal of experimental & clinical cancer research : CR · 2026Article
- METTL16-mediated m6A modification of LYRM2 drives breast cancer progression by inducing CD8Journal of bioenergetics and biomembranes · 2026Article
- METTL14-dependent regulation of HMGB1 attenuates inflammation in diabetic retinopathy.Acta diabetologica · 2026Article
- Loss of METTL3 m6A methyltransferase results in short-term progression and poor treatment outcome of bladder cancer patients.International journal of cancer · 2026Article
- Intratumor microbiota Delftialacustiris correlated with METTL3 to control development of papillary thyroid carcinoma.Cancer cell international · 2026Article
- The METTL3 inhibitor STM2457 suppresses gastric cancer progression by modulating m6A RNA modification.PloS one · 2026Article
394 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMETTL3 is known to be involved in all stages in the life cycle of RNA. It affects the tumor formation by the regulation the m6A modification in the mRNAs of critical oncogenes or tumor suppressors. In bladder cancer, METTL3 could promote the bladder cancer progression via AFF4/NF-κB/MYC signaling network by an m6A dependent manner. Recently, METTL3 was also found to affect the m6A modification in non-coding RNAs including miRNAs, lincRNAs and circRNAs. However, whether this mechanism is related to the proliferation of tumors induced by METTL3 is not reported yet.
methodsQuantitative real-time PCR, western blot and immunohistochemistry were used to detect the expression of METTL3 in bladder cancer. The survival analysis was adopted to explore the association between METTL3 expression and the prognosis of bladder cancer. Bladder cancer cells were stably transfected with lentivirus and cell proliferation and cell cycle, as well as tumorigenesis in nude mice were performed to assess the effect of METTL3 in bladder cancer. RNA immunoprecipitation (RIP), co-immunoprecipitations and RNA m6A dot blot assays were conducted to confirm that METTL3 interacted with the microprocessor protein DGCR8 and modulated the pri-miR221/222 process in an m6A-dependent manner. Luciferase reporter assay was employed to identify the direct binding sites of miR221/222 with PTEN. Colony formation assay and CCK8 assays were conducted to confirm the function of miR-221/222 in METTL3-induced cell growth in bladder cancer.
resultsWe confirmed the oncogenic role of METTL3 in bladder cancer by accelerating the maturation of pri-miR221/222, resulting in the reduction of PTEN, which ultimately leads to the proliferation of bladder cancer. Moreover, we found that METTL3 was significantly increased in bladder cancer and correlated with poor prognosis of bladder cancer patients.
conclusionsOur findings suggested that METTL3 may have an oncogenic role in bladder cancer through interacting with the microprocessor protein DGCR8 and positively modulating the pri-miR221/222 process in an m6A-dependent manner. To our knowledge, this is the first comprehensive study that METTL3 affected the tumor formation by the regulation the m6A modification in non-coding RNAs, which might provide fresh insights into bladder cancer therapy.
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