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• 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?

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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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      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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         Colorectal cancer
         Cell viability
         mTOR
         AZGP1
         Cell migration
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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            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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