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    NPC1 as a Modulator of Disease Severity and Viral Entry of SARSCoV- 2
    (2021)
    VIAL COX, MARIA CECILIA  
    ;
    CALDERON GIADROSIC, JUAN FRANCISCO  
    ;
    KLEIN POSTERNACK, ANDRES DAVID  
    <jats:sec> <jats:title /> <jats:p>The COVID-19 plague is hitting mankind. Several viruses, including SARS-CoV-1, MERS-CoV, EBOV, and SARS-CoV-2, use the endocytic machinery to enter the cell. Genomic variants in NPC1, which encodes for the endo-lysosomal Niemann-Pick type C1 protein, restricts the host-range of viruses in bats and susceptibility to infections in humans. Lack of NPC1 and its pharmacological suppression inhibits many viral infections including SARS-CoV-1 and Type I Feline Coronavirus Infection. Antiviral effects of NPC1-inhibiting drugs for COVID-19 treatment should be explored.</jats:p> </jats:sec>
    Scopus© Citations 10  2
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      1  2Scopus© Citations 56
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    Targeting antisense mitochondrial noncoding RNAs induces bladder cancer cell death and inhibition of tumor growth through reduction of survival and invasion factors
    (2020)
    Vincenzo Borgna
    ;
    Lorena González-sánchez
    ;
    Francisca Guevara
    ;
    Eduardo Landerer
    ;
    Maximiliano Bendek
      10Scopus© Citations 15
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    Exosomes released upon mitochondrial ASncmtRNA knockdown reduce tumorigenic properties of malignant breast cancer cells
    (2020)
    Lorena González-sánchez
    ;
    Rocío Bustos
    ;
    América Campos
    ;
    Valeria Silva
    ;
    Verónica Silva
    <jats:title>Abstract</jats:title><jats:p>During intercellular communication, cells release extracellular vesicles such as exosomes, which contain proteins, ncRNAs and mRNAs that can influence proliferation and/or trigger apoptosis in recipient cells, and have been proposed to play an essential role in promoting invasion of tumor cells and in the preparation of metastatic niches. Our group proposed the antisense non-coding mitochondrial RNA (ASncmtRNA) as a new target for cancer therapy. ASncmtRNA knockdown using an antisense oligonucleotide (ASO-1537S) causes massive death of tumor cells but not normal cells and strongly reduces metastasis in mice. In this work, we report that exosomes derived from ASO-1537S-treated MDA-MB-231 breast cancer cells (Exo-1537S) inhibits tumorigenesis of recipient cells, in contrast to exosomes derived from control-ASO-treated cells (Exo-C) which, in contrast, enhance these properties. Furthermore, an <jats:italic>in vivo</jats:italic> murine peritoneal carcinomatosis model showed that Exo-1537S injection reduced tumorigenicity compared to controls. Proteomic analysis revealed the presence of Lactadherin and VE-Cadherin in exosomes derived from untreated cells (Exo-WT) and Exo-C but not in Exo-1537S, and the latter displayed enrichment of proteasomal subunits. These results suggest a role for these proteins in modulation of tumorigenic properties of exosome-recipient cells. Our results shed light on the mechanisms through which ASncmtRNA knockdown affects the preparation of breast cancer metastatic niches in a peritoneal carcinomatosis model.</jats:p>
      16Scopus© Citations 31