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Author: search.filters.author.Eduardo A. SagredoSubject: search.filters.subject.breast cancer

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    A Comprehensive Analysis of the Effect of A>I(G) RNA-Editing Sites on Genotoxic Drug Response and Progression in Breast Cancer
    (2024)
    Yanara A. Bernal
    ;
    Alejandro Blanco
    ;
    Eduardo A. Sagredo
    ;
    Karen Oróstica  
    ;
    ALFARO CORTEZ, IVAN ESTEBAN  
    Dysregulated A>I(G) RNA editing, which is mainly catalyzed by ADAR1 and is a type of post-transcriptional modification, has been linked to cancer. A low response to therapy in breast cancer (BC) is a significant contributor to mortality. However, it remains unclear if there is an association between A>I(G) RNA-edited sites and sensitivity to genotoxic drugs. To address this issue, we employed a stringent bioinformatics approach to identify differentially RNA-edited sites (DESs) associated with low or high sensitivity (FDR 0.1, log2 fold change 2.5) according to the IC50 of PARP inhibitors, anthracyclines, and alkylating agents using WGS/RNA-seq data in BC cell lines. We then validated these findings in patients with basal subtype BC. These DESs are mainly located in non-coding regions, but a lesser proportion in coding regions showed predicted deleterious consequences. Notably, some of these DESs are previously reported as oncogenic variants, and in genes related to DNA damage repair, drug metabolism, gene regulation, the cell cycle, and immune response. In patients with BC, we uncovered DESs predominantly in immune response genes, and a subset with a significant association (log-rank test p < 0.05) between RNA editing level in LSR, SMPDL3B, HTRA4, and LL22NC03-80A10.6 genes, and progression-free survival. Our findings provide a landscape of RNA-edited sites that may be involved in drug response mechanisms, highlighting the value of A>I(G) RNA editing in clinical outcomes for BC.
    Scopus© Citations 4  7
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    ADAR-Mediated A>I(G) RNA Editing in the Genotoxic Drug Response of Breast Cancer
    (2024)
    Yanara A. Bernal
    ;
    Eduardo Durán
    ;
    Isidora Solar
    ;
    Eduardo A. Sagredo
    ;
    ARMISEN YAÑEZ, RICARDO AMADO  
    <jats:p>Epitranscriptomics is a field that delves into post-transcriptional changes. Among these modifications, the conversion of adenosine to inosine, traduced as guanosine (A&gt;I(G)), is one of the known RNA-editing mechanisms, catalyzed by ADARs. This type of RNA editing is the most common type of editing in mammals and contributes to biological diversity. Disruption in the A&gt;I(G) RNA-editing balance has been linked to diseases, including several types of cancer. Drug resistance in patients with cancer represents a significant public health concern, contributing to increased mortality rates resulting from therapy non-responsiveness and disease progression, representing the greatest challenge for researchers in this field. The A&gt;I(G) RNA editing is involved in several mechanisms over the immunotherapy and genotoxic drug response and drug resistance. This review investigates the relationship between ADAR1 and specific A&gt;I(G) RNA-edited sites, focusing particularly on breast cancer, and the impact of these sites on DNA damage repair and the immune response over anti-cancer therapy. We address the underlying mechanisms, bioinformatics, and in vitro strategies for the identification and validation of A&gt;I(G) RNA-edited sites. We gathered databases related to A&gt;I(G) RNA editing and cancer and discussed the potential clinical and research implications of understanding A&gt;I(G) RNA-editing patterns. Understanding the intricate role of ADAR1-mediated A&gt;I(G) RNA editing in breast cancer holds significant promise for the development of personalized treatment approaches tailored to individual patients’ A&gt;I(G) RNA-editing profiles.</jats:p>
    Scopus© Citations 2  2
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    Scopus© Citations 28  2
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    Increase in ADAR1p110 activates the canonical Wnt signaling pathway associated with aggressive phenotype in triple negative breast cancer cells
    (2022)
    Fernanda Morales
    ;
    Paola Pérez
    ;
    Julio C. Tapia
    ;
    Lorena Lobos-González
    ;
    José Manuel Herranz
      2Scopus© Citations 12