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  1. Analyzed Page
  2. Matching Content Categories
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  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
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We are analyzing https://link.springer.com/article/10.1007/s00018-025-05653-5.

Title:
METTL3-dependent m6A methylation of circCEACAM5 fuels pancreatic cancer progression through DKC1 activation | Cellular and Molecular Life Sciences
Description:
Background Pancreatic 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. Methods circCEACAM5 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. Results circCEACAM5 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. Conclusion METTL3-mediated m6A methylation of circCEACAM5 drives pancreatic cancer progression by increasing DKC1 expression, suggesting potential new therapeutic targets for this aggressive malignancy.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Education
  • Science
  • Health & Fitness

Content Management System {šŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {šŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {šŸ’ø}

We see no obvious way the site makes money.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {šŸ”}

circceacam, cancer, pancreatic, pubmed, cell, cells, analysis, article, dkc, google, scholar, fig, mettl, expression, rna, aspc, cas, central, proliferation, tumor, invasion, progression, apoptosis, overexpression, methylation, migration, data, tissues, assays, circular, promotes, compared, levels, findings, modification, metastasis, performed, knockdown, circrnas, protein, revealed, growth, experiments, rtqpcr, significantly, control, assay, role, presented, ductal,

Topics {āœ’ļø}

regulating hsa-mir-525-3p/mtus2 axis tlr4/nf-Īŗb signaling pathway microrna-182-5p/cyp1a2 pathway mettl3-dependent m6a methylation article download pdf pancreaticĀ ductal adenocarcinoma progression alkbh5-mediated m6a modification mir-338/macc1/met pathway mir-338/macc1/met axis [9] promoting hif-1α transcription mettl3-mediated m6a methylation regulating β-catenin signaling mettl3-induced circ_0008345 contributes protein‒rna complex immunoprecipitation mettl3-mediated m6a modification writing—original draft preparation clinical trait-related m6 hrp-conjugated secondary antibody m6a methylation-mediated circrnas 1 × 10⁹ plaque-forming units m6a-specific rna immunoprecipitation circular rna circ-ldlrad3 analyzing m6a-seq data streptavidin-coated magnetic beads circfoxk2 promotes growth magnetic rna‒protein pull promote chordoma tumorigenesis hrp-linked secondary antibodies exosomal circ-iars 2Ā mg/ml glycine solution rt‒qpcr analysis revealed sh-circceacam5 group relative sirna-mediated mettl3 knockdown predicted rna-binding proteins rna‒protein interaction analysis promoted tumor growth pancreatic ductal adenocarcinoma article zhang increased ki-67-positive cells promotes cell proliferation nf-Īŗb pathway n6-methyladenosine modification investigate rna‒protein interactions rt‒qpcr analysis confirmed ben wei promotes cancer proliferation hpde6-c7 cells performed rt‒qpcr analysis full access 8 μm pore size

Schema {šŸ—ŗļø}

WebPage:
      mainEntity:
         headline:METTL3-dependent m6A methylation of circCEACAM5 fuels pancreatic cancer progression through DKC1 activation
         description:Pancreatic 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. circCEACAM5 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. circCEACAM5 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. METTL3-mediated m6A methylation of circCEACAM5 drives pancreatic cancer progression by increasing DKC1 expression, suggesting potential new therapeutic targets for this aggressive malignancy.
         datePublished:2025-03-27T00:00:00Z
         dateModified:2025-03-27T00:00:00Z
         pageStart:1
         pageEnd:15
         license:http://creativecommons.org/licenses/by-nc-nd/4.0/
         sameAs:https://doi.org/10.1007/s00018-025-05653-5
         keywords:
            Pancreatic cancer
            M6A methylation
            CircCEACAM5
            METTL3
            DKC1
            Cell Biology
            Biomedicine
            general
            Life Sciences
            Biochemistry
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                     name:Nanjing Agricultural University
                     address:
                        name:MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People’s Republic of China
                        type:PostalAddress
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               name:Zihui Qin
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                     name:Nanjing Agricultural University
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                        name:MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People’s Republic of China
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                        name:MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People’s Republic of China
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      headline:METTL3-dependent m6A methylation of circCEACAM5 fuels pancreatic cancer progression through DKC1 activation
      description:Pancreatic 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. circCEACAM5 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. circCEACAM5 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. METTL3-mediated m6A methylation of circCEACAM5 drives pancreatic cancer progression by increasing DKC1 expression, suggesting potential new therapeutic targets for this aggressive malignancy.
      datePublished:2025-03-27T00:00:00Z
      dateModified:2025-03-27T00:00:00Z
      pageStart:1
      pageEnd:15
      license:http://creativecommons.org/licenses/by-nc-nd/4.0/
      sameAs:https://doi.org/10.1007/s00018-025-05653-5
      keywords:
         Pancreatic cancer
         M6A methylation
         CircCEACAM5
         METTL3
         DKC1
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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                     name:Jining First People’s Hospital, Jining Medical University, Jining, People’s Republic of China
                     type:PostalAddress
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            name:Wenda Wu
            affiliation:
                  name:Nanjing Agricultural University
                  address:
                     name:MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People’s Republic of China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Zihui Qin
            affiliation:
                  name:Nanjing Agricultural University
                  address:
                     name:MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People’s Republic of China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Ben Wei
            affiliation:
                  name:Nanjing Agricultural University
                  address:
                     name:MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People’s Republic of China
                     type:PostalAddress
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                  name:Changshu Institute of Technology
                  address:
                     name:School of Biology and Food Engineering, Changshu Institute of Technology, Suzhou, People’s Republic of China
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            address:
               name:School of Biology and Food Engineering, Changshu Institute of Technology, Suzhou, People’s Republic of China
               type:PostalAddress
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      name:Wenxue Sun
      affiliation:
            name:Jining First People’s Hospital, Jining Medical University
            address:
               name:Jining First People’s Hospital, Jining Medical University, Jining, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Wenda Wu
      affiliation:
            name:Nanjing Agricultural University
            address:
               name:MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Zihui Qin
      affiliation:
            name:Nanjing Agricultural University
            address:
               name:MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Ben Wei
      affiliation:
            name:Nanjing Agricultural University
            address:
               name:MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Tushuai Li
      url:http://orcid.org/0000-0002-6219-1397
      affiliation:
            name:Changshu Institute of Technology
            address:
               name:School of Biology and Food Engineering, Changshu Institute of Technology, Suzhou, People’s Republic of China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:School of Biology and Food Engineering, Changshu Institute of Technology, Suzhou, People’s Republic of China
      name:Jining First People’s Hospital, Jining Medical University, Jining, People’s Republic of China
      name:MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People’s Republic of China
      name:MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People’s Republic of China
      name:MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People’s Republic of China
      name:School of Biology and Food Engineering, Changshu Institute of Technology, Suzhou, People’s Republic of China

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