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  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
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We began analyzing https://link.springer.com/article/10.1007/s00018-023-04833-5, but it redirected us to https://link.springer.com/article/10.1007/s00018-023-04833-5. The analysis below is for the second page.

Title[redir]:
DIS3L2 knockdown impairs key oncogenic properties of colorectal cancer cells via the mTOR signaling pathway | Cellular and Molecular Life Sciences
Description:
DIS3L2 degrades different types of RNAs in an exosome-independent manner including mRNAs and several types of non-coding RNAs. DIS3L2-mediated degradation is preceded by the addition of nontemplated uridines at the 3’end of its targets by the terminal uridylyl transferases 4 and 7. Most of the literature that concerns DIS3L2 characterizes its involvement in several RNA degradation pathways, however, there is some evidence that its dysregulated activity may contribute to cancer development. In the present study, we characterize the role of DIS3L2 in human colorectal cancer (CRC). Using the public RNA datasets from The Cancer Genome Atlas (TCGA), we found higher DIS3L2 mRNA levels in CRC tissues versus normal colonic samples as well as worse prognosis in patients with high DIS3L2 expression. In addition, our RNA deep-sequencing data revealed that knockdown (KD) of DIS3L2 induces a strong transcriptomic disturbance in SW480 CRC cells. Moreover, gene ontology (GO) analysis of significant upregulated transcripts displays enrichment in mRNAs encoding proteins involved in cell cycle regulation and cancer-related pathways, which guided us to evaluate which specific hallmarks of cancer are differentially regulated by DIS3L2. To do so, we employed four CRC cell lines (HCT116, SW480, Caco-2 and HT-29) differing in their mutational background and oncogenicity. We demonstrate that depletion of DIS3L2 results in reduced cell viability of highly oncogenic SW480 and HCT116 CRC cells, but had little or no impact in the more differentiated Caco-2 and HT-29 cells. Remarkably, the mTOR signaling pathway, crucial for cell survival and growth, is downregulated after DIS3L2 KD, whereas AZGP1, an mTOR pathway inhibitor, is upregulated. Furthermore, our results indicate that depletion of DIS3L2 disturbs metastasis-associated properties, such as cell migration and invasion, only in highly oncogenic CRC cells. Our work reveals for the first time a role for DIS3L2 in sustaining CRC cell proliferation and provides evidence that this ribonuclease is required to support the viability and invasive behavior of dedifferentiated CRC cells.

Matching Content Categories {📚}

  • Science
  • Education
  • Telecommunications

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org 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 Doi.org Make Money? {💸}

We can't figure out the monetization strategy.

Not every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Doi.org could be secretly minting cash, but we can't detect the process.

Keywords {🔍}

disl, cells, cell, pubmed, article, cancer, google, scholar, fig, control, crc, expression, analysis, pathway, mrna, gene, viability, depletion, central, mtor, levels, tuts, hct, condition, data, results, lines, rna, rnaseq, cas, migration, supplementary, role, significant, conditions, azgp, upregulated, colorectal, transcripts, knockdown, genes, proliferation, tumor, performed, observed, signaling, caco, ncm, overexpression, human,

Topics {✒️}

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Questions {❓}

  • Belfiore A, Rapicavoli RV, Le Moli R et al (2023) IGF2: a role in metastasis and tumor evasion from immune surveillance?
  • Thornton JE, Gregory RI (2012) How does Lin28 let-7 control development and disease?

Schema {🗺️}

WebPage:
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         headline:DIS3L2 knockdown impairs key oncogenic properties of colorectal cancer cells via the mTOR signaling pathway
         description:DIS3L2 degrades different types of RNAs in an exosome-independent manner including mRNAs and several types of non-coding RNAs. DIS3L2-mediated degradation is preceded by the addition of nontemplated uridines at the 3’end of its targets by the terminal uridylyl transferases 4 and 7. Most of the literature that concerns DIS3L2 characterizes its involvement in several RNA degradation pathways, however, there is some evidence that its dysregulated activity may contribute to cancer development. In the present study, we characterize the role of DIS3L2 in human colorectal cancer (CRC). Using the public RNA datasets from The Cancer Genome Atlas (TCGA), we found higher DIS3L2 mRNA levels in CRC tissues versus normal colonic samples as well as worse prognosis in patients with high DIS3L2 expression. In addition, our RNA deep-sequencing data revealed that knockdown (KD) of DIS3L2 induces a strong transcriptomic disturbance in SW480 CRC cells. Moreover, gene ontology (GO) analysis of significant upregulated transcripts displays enrichment in mRNAs encoding proteins involved in cell cycle regulation and cancer-related pathways, which guided us to evaluate which specific hallmarks of cancer are differentially regulated by DIS3L2. To do so, we employed four CRC cell lines (HCT116, SW480, Caco-2 and HT-29) differing in their mutational background and oncogenicity. We demonstrate that depletion of DIS3L2 results in reduced cell viability of highly oncogenic SW480 and HCT116 CRC cells, but had little or no impact in the more differentiated Caco-2 and HT-29 cells. Remarkably, the mTOR signaling pathway, crucial for cell survival and growth, is downregulated after DIS3L2 KD, whereas AZGP1, an mTOR pathway inhibitor, is upregulated. Furthermore, our results indicate that depletion of DIS3L2 disturbs metastasis-associated properties, such as cell migration and invasion, only in highly oncogenic CRC cells. Our work reveals for the first time a role for DIS3L2 in sustaining CRC cell proliferation and provides evidence that this ribonuclease is required to support the viability and invasive behavior of dedifferentiated CRC cells.
         datePublished:2023-06-20T00:00:00Z
         dateModified:2023-06-20T00:00:00Z
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      headline:DIS3L2 knockdown impairs key oncogenic properties of colorectal cancer cells via the mTOR signaling pathway
      description:DIS3L2 degrades different types of RNAs in an exosome-independent manner including mRNAs and several types of non-coding RNAs. DIS3L2-mediated degradation is preceded by the addition of nontemplated uridines at the 3’end of its targets by the terminal uridylyl transferases 4 and 7. Most of the literature that concerns DIS3L2 characterizes its involvement in several RNA degradation pathways, however, there is some evidence that its dysregulated activity may contribute to cancer development. In the present study, we characterize the role of DIS3L2 in human colorectal cancer (CRC). Using the public RNA datasets from The Cancer Genome Atlas (TCGA), we found higher DIS3L2 mRNA levels in CRC tissues versus normal colonic samples as well as worse prognosis in patients with high DIS3L2 expression. In addition, our RNA deep-sequencing data revealed that knockdown (KD) of DIS3L2 induces a strong transcriptomic disturbance in SW480 CRC cells. Moreover, gene ontology (GO) analysis of significant upregulated transcripts displays enrichment in mRNAs encoding proteins involved in cell cycle regulation and cancer-related pathways, which guided us to evaluate which specific hallmarks of cancer are differentially regulated by DIS3L2. To do so, we employed four CRC cell lines (HCT116, SW480, Caco-2 and HT-29) differing in their mutational background and oncogenicity. We demonstrate that depletion of DIS3L2 results in reduced cell viability of highly oncogenic SW480 and HCT116 CRC cells, but had little or no impact in the more differentiated Caco-2 and HT-29 cells. Remarkably, the mTOR signaling pathway, crucial for cell survival and growth, is downregulated after DIS3L2 KD, whereas AZGP1, an mTOR pathway inhibitor, is upregulated. Furthermore, our results indicate that depletion of DIS3L2 disturbs metastasis-associated properties, such as cell migration and invasion, only in highly oncogenic CRC cells. Our work reveals for the first time a role for DIS3L2 in sustaining CRC cell proliferation and provides evidence that this ribonuclease is required to support the viability and invasive behavior of dedifferentiated CRC cells.
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      dateModified:2023-06-20T00:00:00Z
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      keywords:
         DIS3L2
         Colorectal cancer
         Cell viability
         mTOR
         AZGP1
         Cell migration
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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            address:
               name:Faculdade de Ciências, BioISI – Instituto de Biossistemas e Ciências Integrativas, Universidade de Lisboa, Lisbon, Portugal
               type:PostalAddress
            type:Organization
      name:Paulo J. da Costa
      affiliation:
            name:Instituto Nacional de Saúde Doutor Ricardo Jorge
            address:
               name:Departamento de Genética Humana, Instituto Nacional de Saúde Doutor Ricardo Jorge, Lisbon, Portugal
               type:PostalAddress
            type:Organization
            name:Universidade de Lisboa
            address:
               name:Faculdade de Ciências, BioISI – Instituto de Biossistemas e Ciências Integrativas, Universidade de Lisboa, Lisbon, Portugal
               type:PostalAddress
            type:Organization
      name:Marcelo Pereira
      affiliation:
            name:Universidade de Lisboa
            address:
               name:Faculdade de Ciências, BioISI – Instituto de Biossistemas e Ciências Integrativas, Universidade de Lisboa, Lisbon, Portugal
               type:PostalAddress
            type:Organization
      name:Margarida Gama-Carvalho
      affiliation:
            name:Universidade de Lisboa
            address:
               name:Faculdade de Ciências, BioISI – Instituto de Biossistemas e Ciências Integrativas, Universidade de Lisboa, Lisbon, Portugal
               type:PostalAddress
            type:Organization
      name:Paulo Matos
      affiliation:
            name:Instituto Nacional de Saúde Doutor Ricardo Jorge
            address:
               name:Departamento de Genética Humana, Instituto Nacional de Saúde Doutor Ricardo Jorge, Lisbon, Portugal
               type:PostalAddress
            type:Organization
            name:Universidade de Lisboa
            address:
               name:Faculdade de Ciências, BioISI – Instituto de Biossistemas e Ciências Integrativas, Universidade de Lisboa, Lisbon, Portugal
               type:PostalAddress
            type:Organization
      name:Luísa Romão
      url:http://orcid.org/0000-0002-5061-5287
      affiliation:
            name:Instituto Nacional de Saúde Doutor Ricardo Jorge
            address:
               name:Departamento de Genética Humana, Instituto Nacional de Saúde Doutor Ricardo Jorge, Lisbon, Portugal
               type:PostalAddress
            type:Organization
            name:Universidade de Lisboa
            address:
               name:Faculdade de Ciências, BioISI – Instituto de Biossistemas e Ciências Integrativas, Universidade de Lisboa, Lisbon, Portugal
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Departamento de Genética Humana, Instituto Nacional de Saúde Doutor Ricardo Jorge, Lisbon, Portugal
      name:Faculdade de Ciências, BioISI – Instituto de Biossistemas e Ciências Integrativas, Universidade de Lisboa, Lisbon, Portugal
      name:Departamento de Genética Humana, Instituto Nacional de Saúde Doutor Ricardo Jorge, Lisbon, Portugal
      name:Faculdade de Ciências, BioISI – Instituto de Biossistemas e Ciências Integrativas, Universidade de Lisboa, Lisbon, Portugal
      name:Departamento de Genética Humana, Instituto Nacional de Saúde Doutor Ricardo Jorge, Lisbon, Portugal
      name:Faculdade de Ciências, BioISI – Instituto de Biossistemas e Ciências Integrativas, Universidade de Lisboa, Lisbon, Portugal
      name:Faculdade de Ciências, BioISI – Instituto de Biossistemas e Ciências Integrativas, Universidade de Lisboa, Lisbon, Portugal
      name:Faculdade de Ciências, BioISI – Instituto de Biossistemas e Ciências Integrativas, Universidade de Lisboa, Lisbon, Portugal
      name:Departamento de Genética Humana, Instituto Nacional de Saúde Doutor Ricardo Jorge, Lisbon, Portugal
      name:Faculdade de Ciências, BioISI – Instituto de Biossistemas e Ciências Integrativas, Universidade de Lisboa, Lisbon, Portugal
      name:Departamento de Genética Humana, Instituto Nacional de Saúde Doutor Ricardo Jorge, Lisbon, Portugal
      name:Faculdade de Ciências, BioISI – Instituto de Biossistemas e Ciências Integrativas, Universidade de Lisboa, Lisbon, Portugal

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