ALFARO CORTEZ, IVAN ESTEBAN
Preferred name
ALFARO CORTEZ, IVAN ESTEBAN
Main Affiliation
ORCID
0000-0002-5938-5940
Scopus Author ID
24066581500
12 results
Now showing 1 - 10 of 12
- Some of the metrics are blocked by yourconsent settings
Item type:Publication, A Comprehensive Analysis of the Effect of A>I(G) RNA-Editing Sites on Genotoxic Drug Response and Progression in Breast Cancer(2024); 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 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Chaperone Mediated Autophagy Degrades TDP-43 Protein and Is Affected by TDP-43 Aggregation(2020); 2Scopus© Citations 61 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, PKR-driven ISR signaling controls synaptic translation and structural plasticity in an age-dependent manner(Elsevier BV, 2025-11)Scopus© Citations 2 2 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Connexin-46 Contained in Extracellular Vesicles Enhance Malignancy Features in Breast Cancer Cells(2020); ; <jats:p>Under normal conditions, almost all cell types communicate with their neighboring cells through gap junction channels (GJC), facilitating cellular and tissue homeostasis. A GJC is formed by the interaction of two hemichannels; each one of these hemichannels in turn is formed by six subunits of transmembrane proteins called connexins (Cx). For many years, it was believed that the loss of GJC-mediated intercellular communication was a hallmark in cancer development. However, nowadays this paradigm is changing. The connexin 46 (Cx46), which is almost exclusively expressed in the eye lens, is upregulated in human breast cancer, and is correlated with tumor growth in a Xenograft mouse model. On the other hand, extracellular vesicles (EVs) have an important role in long-distance communication under physiological conditions. In the last decade, EVs also have been recognized as key players in cancer aggressiveness. The aim of this work was to explore the involvement of Cx46 in EV-mediated intercellular communication. Here, we demonstrated for the first time, that Cx46 is contained in EVs released from breast cancer cells overexpressing Cx46 (EVs-Cx46). This EV-Cx46 facilitates the interaction between EVs and the recipient cell resulting in an increase in their migration and invasion properties. Our results suggest that EV-Cx46 could be a marker of cancer malignancy and open the possibility to consider Cx46 as a new therapeutic target in cancer treatment.</jats:p>3Scopus© Citations 29 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Extracellular Cysteines Are Critical to Form Functional Cx46 Hemichannels(2022)2Scopus© Citations 6 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Palmitic and Stearic Acids Inhibit Chaperone-Mediated Autophagy (CMA) in POMC-like Neurons In Vitro(2022)Scopus© Citations 7 3 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, KFERQ-selective protein autophagy in Caenorhabditis elegans depends on LMP-1(Public Library of Science (PLoS), 2025-09-02); ; Carlos F. LagosMammalian cells exhibit three autophagy mechanisms: macroautophagy, microautophagy (MIA), and chaperone-mediated autophagy (CMA), each employing unique mechanisms for transporting cellular material to the lysosome for degradation. MIA involves the engulfment of proteins via lysosomes/late endosomes through membrane invagination, while CMA directly imports cytosolic proteins into lysosomes, selectively targeting those harboring the KFERQ pentapeptide motif, helped by the chaperone HSC70. Despite the identification of several genetic markers of these pathways, our understanding of the underlying mechanisms, particularly in MIA and CMA, remains limited. To study CMA in vivo we designed a photoactivatable CMA reporter consisting of a plasmid encoding the KFERQ consensus signal for CMA targeting. We generated transgenic <jats:italic><jats:italic>C. elegans</jats:italic></jats:italic> strains with diverse genetic backgrounds to analyze the role of known molecular components of CMA in mammals. Additionally, we conducted an in-silico analysis of the structural interaction between <jats:italic><jats:italic>C. elegans</jats:italic></jats:italic> LMP-1 or LMP-2 proteins with the HSP-1 chaperone. Results: Our study shows a significant alteration in the distribution pattern of the KFERQ reporter in muscle cells upon induction of selective autophagy (CMA or MIA). We found that the reporter localized into lysosomes only during starvation, which abrogated in the absence of LMP-1. This study validates CMA in <jats:italic><jats:italic>C. elegans</jats:italic></jats:italic> and provides the development of a new tool for understanding selective autophagy mechanisms and their potential implications in various organisms.1Scopus© Citations 2 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Chaperone mediated autophagy contributes to the newly synthesized histones H3 and H4 quality control(2022); 4Scopus© Citations 16 - Some of the metrics are blocked by yourconsent settings
Item type:Product, Dataset - A Comprehensive Analysis of the Effect of A>I(G) RNA-Editing Sites on Genotoxic Drug Response and Progression in Breast Cancer(GITHUB, 2024); ; ALEJANDRO BLANCO2 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Cx40 Levels Regulate Hypoxia-Induced Changes in the Migration, Proliferation, and Formation of Gap Junction Plaques in an Extravillous Trophoblast Cell Model(2024)2Scopus© Citations 2