ArticleCellular and molecular life sciences : CMLS2025
METTL3-dependent m6A methylation of circCEACAM5 fuels pancreatic cancer progression through DKC1 activation.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- RNA methyltransferase 3 drives pancreatic acinar cell carcinoma growth and is a therapeutic target.Signal transduction and targeted therapy · 2026Article
- GPSM2 Promotes Pancreatic Cancer Progression Through METTL3-Mediated m6A Modification of YAP1 mRNA.Journal of cellular and molecular medicine · 2026Article
- Interplay of RNA mFASEB bioAdvances · 2026Article
- ALKBH5 facilitates Srgn stability via m6A demethylation to disrupt blood-testis barrier integrity in the high-fat diet mice.Cellular and molecular life sciences : CMLS · 2026Article
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- m6A RNA modification and its emerging roles in diseases: recent advances and therapeutic implications.Journal of translational medicine · 2026Review
- Hsa_circ_PCNT sponges hsa-miR-133b to promote SHH medulloblastoma via TAGLN2.Cellular and molecular life sciences : CMLS · 2026Article
- Multidimensional regulatory roles and therapeutic applications of SRSF7 in cancer.Cell death discovery · 2025Review
- Recent advances of circular RNAs in gastrointestinal cancer.World journal of clinical oncology · 2025Review
- Novel insights into the N 6-methyladenosine modification on circRNA in cancer.Frontiers in oncology · 2025Review
- METTL3-mediated circ_0003998 serves as oncogene in non-small cell lung cancer through regulating miR-330-5p/CXCL3 axis.Cell cycle (Georgetown, Tex.)Article
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6 authors.
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Abstract
backgroundPancreatic cancer is highly lethal and has a poor prognosis. Research has highlighted the role of circular RNAs and m6A methylation in cancer progression. METTL3, a key m6A methyltransferase, is linked to various cancers, but its interaction with circular RNAs in pancreatic cancer is unclear. This study examined the role of circCEACAM5 in pancreatic cancer, particularly its regulation by METTL3-mediated m6A methylation and interaction with effectors such as DKC1.
methodscircCEACAM5 expression in pancreatic cancer tissues and cell lines was evaluated via RT‒qPCR. Its characteristics were validated through Sanger sequencing, stability assays, and FISH. Functional assays (CCK-8, EdU, Transwell, and flow cytometry) were conducted in AsPC-1 cells, and in vivo tumor models were established. m6A modification was analyzed via bioinformatics tools and m6A-specific immunoprecipitation, while RNA pull-down assays were used to examine the interaction of circCEACAM5 with METTL3 and DKC1.
resultscircCEACAM5 was significantly upregulated in pancreatic cancer and correlated with poor clinical outcomes. CircCEACAM5 promoted cell proliferation, invasion, and migration while inhibiting apoptosis both in vitro and in vivo. METTL3-mediated m6A methylation of circCEACAM5 was confirmed, and METTL3 knockdown reversed the effects of circCEACAM5 silencing on the malignant behavior of pancreatic cancer cells. circCEACAM5 interacted with DKC1, and DKC1 overexpression reversed the effects of circCEACAM5 knockdown on the malignant behavior of pancreatic cancer cells.
conclusionMETTL3-mediated m6A methylation of circCEACAM5 drives pancreatic cancer progression by increasing DKC1 expression, suggesting potential new therapeutic targets for this aggressive malignancy.
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