Grupos Investigadores

Miembros del Grupo

Coordinador
Fortes , Puri
(pfortes@unav.es)
Investigadores
Marina
Barriocanal Urbina
Celia
Prior Darbonnens
Colaboradores
Nerea
Razquin Erro
Eric
Rovira Barreira
Beatriz
Suarez Alvarez
Juan Pablo
Unfried Huertas

Líneas de Investigación

  • Caracterización funcional de RNAs largos no codificantes que se inducen en respuesta a interferón o a infección viral
  • Estudio mecanístico y traslacional del efecto del ácido docosahexanoico en la actividad de las células estrelladas hepáticas
  • Identificación de nuevos mecanismos de regulación de la expresión génica
  • Identificación y análisis funcional del RNAs lasgos no codificantes implicados en la iniciación o el desarrollo del hepatocarcinoma

Palabras Clave

  • Cirrosis
  • Células estelares
  • Estrés celular
  • Hepatocarcinoma
  • Hígado
  • IFN
  • LncRNAs
  • NFKB
  • Regulación expresión génica
  • Respuesta antiviral
  • Ácido docosahexanoico

Publicaciones Científicas desde 2018

  • Autores: de Braganc, S.; Aicart-Ramos, C.; Arribas-Bosacoma, R.; et al.
    Revista: CELL REPORTS
    ISSN: 2211-1247 Vol.42 N° 1 2023 págs. 111917
    Resumen
    The synapsis of DNA ends is a critical step for the repair of double-strand breaks by non-homologous end joining (NHEJ). This is performed by a multicomponent protein complex assembled around Ku70-Ku80 heterodimers and regulated by accessory factors, including long non-coding RNAs, through poorly understood mechanisms. Here, we use magnetic tweezers to investigate the contributions of core NHEJ proteins and APLF and lncRNA NIHCOLE to DNA synapsis. APLF stabilizes DNA end bridging and, together with Ku70-Ku80, establishes a minimal complex that supports DNA synapsis for several minutes under piconewton forces. We find the C-terminal acidic region of APLF to be critical for bridging. NIHCOLE increases the dwell time of the synapses by Ku70-Ku80 and APLF. This effect is further enhanced by a small and structured RNA domain within NIHCOLE. We propose a model where Ku70-Ku80 can simultaneously bind DNA, APLF, and structured RNAs to promote the stable joining of DNA ends.
  • Autores: Barriocanal Urbina, Marina; Prats Mari, Laura; Razquin Erro, Nerea; et al.
    Revista: FRONTIERS IN IMMUNOLOGY
    ISSN: 1664-3224 Vol.13 2022 págs. 829335
    Resumen
    The study of the interferon (IFN) alpha-induced cell transcriptome has shown altered expression of several long non-coding RNAs (lncRNAs). ISR8/IRF1-AS1 (IFN stimulated RNA 8), located close to IFN regulatory factor 1 (IRF1) coding gene, transcribes a lncRNA induced at early times after IFN alpha treatment or IRF1 or NF-kappa B activation. Depletion or overexpression of ISR8 RNA does not lead to detected deregulation of the IFN response. Surprisingly, disruption of ISR8 locus with CRISPR-Cas9 genome editing results in cells that fail to induce several key ISGs and pro-inflammatory cytokines after a trigger with IFN alpha or overexpression of IRF1 or the NF-kappa B subunit RELA. This suggests that the ISR8 locus may play a relevant role in IFN alpha and NF-kappa B pathways. Interestingly, IFN alpha, IRFs and NF-kappa B-responding luciferase reporters are normally induced in ISR8-disrupted cells when expressed from a plasmid but not when integrated into the genome. Therefore, IFN alpha and NF-kappa B pathways are functional to induce the expression of exogenous episomic transcripts but fail to activate transcription from genomic promoters. Transcription from these promoters is not restored with silencing inhibitors, by decreasing the levels of several negative regulators or by overexpression of inducers. Transcriptome analyses indicate that ISR8-disrupted cells have a drastic increase in the levels of negative regulators such as XIST and Zinc finger proteins. Our results agree with ISR8 loci being an enhancer region that is fundamental for proper antiviral and proinflammatory responses. These results are relevant because several SNPs located in the ISR8 region are associated with chronic inflammatory and autoimmune diseases including Crohn's disease, inflammatory bowel disease, ulcerative colitis or asthma.
  • Autores: Rovira Barreira, Eric; Moreno Bruna, Beatriz; Razquin Erro, Nerea; et al.
    Revista: MOLECULAR THERAPY - NUCLEIC ACIDS
    ISSN: 2162-2531 Vol.28 2022 págs. 831 - 846
    Resumen
    Here, we show that direct recruitment of U1A to target transcripts can increase gene expression. This is a new regulatory role, in addition to previous knowledge showing that U1A decreases the levels of U1A mRNA and other specific targets. In fact, genome-wide, U1A more often increases rather than represses gene expression and many U1A-upregulated transcripts are directly bound by U1A according to individual nucleotide resolution crosslinking and immunoprecipitation (iCLIP) studies. Interestingly, U1A-mediated positive regulation can be transferred to a heterologous system for biotechnological purposes. Finally, U1A-bound genes are enriched for those involved in cell cycle and adhesion. In agreement with this, higher U1A mRNA expression associates with lower disease-free survival and overall survival in many cancer types, and U1A mRNA levels positively correlate with those of some oncogenes involved in cell proliferation. Accordingly, U1A depletion leads to decreased expression of these genes and the migration-related gene CCN2/CTGF, which shows the strongest regulation by U1A. A decrease in U1A causes a strong drop in CCN2 expression and CTGF secretion and defects in the expression of CTGF EMT targets, cell migration, and proliferation. These results support U1A as a putative therapeutic target for cancer treatment. In addition, U1A-binding sequences should be considered in biotechnological applications.
  • Autores: Unfried Huertas, Juan Pablo (Autor de correspondencia); Sangro del Alcazar, Paloma (Autor de correspondencia); Prats Mari, Laura; et al.
    Revista: CANCERS
    ISSN: 2072-6694 Vol.13 N° 11 2021 págs. 2651
    Resumen
    Simple Summary Hepatocellular carcinoma is the major form of liver cancer; it has a high incidence in the global population, and it is a leading cause of the world's cancer burden. Despite great efforts to understand the disease at the molecular level and develop effective treatments for hepatocellular carcinoma patients, current therapies for advanced cases are only effective in a small percentage of patients. Therefore, it is paramount to discover new tumor targets that can be used to develop alternative therapeutic strategies. Promising novel targets could be long non-coding RNAs. These RNA molecules are frequently found to be involved in the development and progression of cancer. More importantly, they can be safely targeted with several strategies. However, our knowledge about long non-coding RNA biology and their clinical relevance remains underdeveloped. In this review, we summarize current efforts to validate the importance of long non-coding RNAs in hepatocellular carcinoma and to evaluate their potential to impact the clinical setting. To do that we highlight lncRNA implication in key events leading to cancer and we describe how affecting lncRNAs could broaden the repertoire of potentially useful targets to help meet the challenge of hepatocellular carcinoma treatment. LncRNAs are emerging as relevant regulators of multiple cellular processes involved in cell physiology as well as in the development and progression of human diseases, most notably, cancer. Hepatocellular carcinoma (HCC) is a prominent cause of cancer-related death worldwide due to the high prevalence of causative factors, usual cirrhotic status of the tumor-harboring livers and the suboptimal benefit of locoregional and systemic therapies. Despite huge progress in the molecular characterization of HCC, no oncogenic loop addiction has been identified and most genetic alterations remain non-druggable, underscoring the importance of advancing research in novel approaches for HCC treatment. In this context, long non-coding RNAs (lncRNAs) appear as potentially useful targets as they often exhibit high tumor- and tissue-specific expression and many studies have reported an outstanding dysregulation of lncRNAs in HCC. However, there is a limited perspective of the potential role that deregulated lncRNAs may play in HCC progression and aggressiveness or the mechanisms and therapeutic implications behind such effects. In this review, we offer a clarifying landscape of current efforts to evaluate lncRNA potential as therapeutic targets in HCC using evidence from preclinical models as well as from recent studies on novel oncogenic pathways that show lncRNA-dependency.
  • Autores: Izadirad, M.; Jafari, L.; James, A. R.; et al.
    Revista: DRUG DISCOVERY TODAY
    ISSN: 1359-6446 Vol.26 N° 7 2021 págs. 1735 - 1743
    Resumen
    Many patients with acute myeloid leukemia (AML) experience poor outcomes following traditional high-dose chemotherapies and complete remission rates remain suboptimal. Chemoresistance is an obstacle to effective chemotherapy and the precise mechanisms involved remain to be determined. Recently, long noncoding RNAs (lncRNAs) have been identified as relevant factors in the development of drug resistance in patients with AML. Furthermore, accumulating data support the importance of lncRNAs as potentially useful novel therapeutic targets in many cancers. Here, we review the role of lncRNAs in the development and induction of the chemoresistance in AML, and suggest lncRNAs as novel molecular markers for diagnosis, prediction of patient response to chemotherapy, and novel therapeutic targets for AML.
  • Autores: Cable, J.; Heard, E. (Autor de correspondencia); Hirose, T.; et al.
    Revista: ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
    ISSN: 0077-8923 Vol.1506 N° 1 2021 págs. 118 - 141
    Resumen
    The human transcriptome contains many types of noncoding RNAs, which rival the number of protein-coding species. From long noncoding RNAs (lncRNAs) that are over 200 nucleotides long to piwi-interacting RNAs (piRNAs) of only 20 nucleotides, noncoding RNAs play important roles in regulating transcription, epigenetic modifications, translation, and cell signaling. Roles for noncoding RNAs in disease mechanisms are also being uncovered, and several species have been identified as potential drug targets. On May 11-14, 2021, the Keystone eSymposium Noncoding RNAs: Biology and Applications brought together researchers working in RNA biology, structure, and technologies to accelerate both the understanding of RNA basic biology and the translation of those findings into clinical applications.
  • Autores: Unfried Huertas, Juan Pablo; Marín-Baquero, M.; Rivera-Calzada, A.; et al.
    Revista: CANCER RESEARCH
    ISSN: 0008-5472 Vol.81 N° 19 2021 págs. 4910 - 4925
    Resumen
    Long noncoding RNAs (lncRNA) are emerging as key players in cancer as parts of poorly understood molecular mechanisms. Here, we investigated lncRNAs that play a role in hepatocellular carcinoma (HCC) and identified NIHCOLE, a novel lncRNA induced in HCC with oncogenic potential and a role in the ligation efficiency of DNA double-stranded breaks (DSB). NIHCOLE expression was associated with poor prognosis and survival of HCC patients. Depletion of NIHCOLE from HCC cells led to impaired proliferation and increased apoptosis. NIHCOLE deficiency led to accumulation of DNA damage due to a specific decrease in the activity of the nonhomologous end-joining (NHEJ) pathway of DSB repair. DNA damage induction in NIHCOLE-depleted cells further decreased HCC cell growth. NIHCOLE was associated with DSB markers and recruited several molecules of the Ku70/Ku80 heterodimer. Further, NIHCOLE putative structural domains supported stable multimeric complexes formed by several NHEJ factors including Ku70/80, APLF, XRCC4, and DNA ligase IV. NHEJ reconstitution assays showed that NIHCOLE promoted the ligation efficiency of bluntended DSBs. Collectively, these data show that NIHCOLE serves as a scaffold and facilitator of NHEJ machinery and confers an advantage to HCC cells, which could be exploited as a targetable vulnerability. Significance: This study characterizes the role of lncRNA NIHCOLE in DNA repair and cellular fitness in HCC, thus implicating it as a therapeutic target.
  • Autores: Barriocanal Urbina, Marina; Prior Darbonnens, Celia; Suarez Alvarez, Beatriz; et al.
    Revista: JOURNAL OF IMMUNOLOGY
    ISSN: 0022-1767 Vol.206 N° 8 2021 págs. 1932 - 1942
    Resumen
    The cell has several mechanisms to sense and neutralize stress. Stress-related stimuli activate pathways that counteract danger, support cell survival, and activate the inflammatory response. We use human cells to show that these processes are modulated by EGOT, a long noncoding RNA highly induced by viral infection, whose inhibition results in increased levels of antiviral IFNstimulated genes (ISGs) and decreased viral replication. We now show that EGOT is induced in response to cell stress, viral replication, or the presence of pathogen-associated molecular patterns via the PI3K/AKT, MAPKs, and NF-kappa B pathways, which lead to cell survival and inflammation. Transcriptome analysis and validation experiments show that EGOT modulates PI3K/AKT and NF-kappa B responses. On the one hand, EGOT inhibition decreases expression of PI3K/AKT-induced cellular receptors and cell proliferation. In fact, EGOT levels are increased in several tumors. On the other hand, EGOT inhibition results in decreased levels of key NF-kappa B target genes, including those required for inflammation and ISGs in those cells that build an antiviral response. Mechanistically, EGOT depletion decreases the levels of the key coactivator TBLR1, essential for transcription by NF-kappa B. In summary, EGOT is induced in response to stress and may function as a switch that represses ISG transcription until a proper antiviral or stress response is initiated. EGOT then helps PI3K/AKT, MAPKs, and NF-kappa B pathways to activate the antiviral response, cell inflammation, and growth. We believe that modulation of EGOT levels could be used as a therapy for the treatment of certain viral infections, immune diseases, and cancer.
  • Autores: Suarez, B; Prats-Mari, L; Unfried Huertas, Juan Pablo (Autor de correspondencia); et al.
    Revista: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
    ISSN: 1422-0067 Vol.21 N° 17 2020
    Resumen
    The proper functioning of the immune system requires a robust control over a delicate equilibrium between an ineffective response and immune overactivation. Poor responses to viral insults may lead to chronic or overwhelming infection, whereas unrestrained activation can cause autoimmune diseases and cancer. Control over the magnitude and duration of the antiviral immune response is exerted by a finely tuned positive or negative regulation at the DNA, RNA, and protein level of members of the type I interferon (IFN) signaling pathways and on the expression and activity of antiviral and proinflammatory factors. As summarized in this review, committed research during the last decade has shown that several of these processes are exquisitely regulated by long non-coding RNAs (lncRNAs), transcripts with poor coding capacity, but highly versatile functions. After infection, viruses, and the antiviral response they trigger, deregulate the expression of a subset of specific lncRNAs that function to promote or repress viral replication by inactivating or potentiating the antiviral response, respectively. These IFN-related lncRNAs are also highly tissue- and cell-type-specific, rendering them as promising biomarkers or therapeutic candidates to modulate specific stages of the antiviral immune response with fewer adverse effects.
  • Autores: Unfried Huertas, Juan Pablo; Fortes, Puri
    Revista: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
    ISSN: 1422-0067 Vol.21 N° 6 2020 págs. 2255
    Resumen
    Long non-coding RNAs (lncRNAs) are transcripts with poor coding capacity that may interact with proteins, DNA, or other RNAs to perform structural and regulatory functions. The lncRNA transcriptome changes significantly in most diseases, including cancer and viral infections. In this review, we summarize the functional implications of lncRNA-deregulation after infection with hepatitis C virus (HCV). HCV leads to chronic infection in many patients that may progress to liver cirrhosis and hepatocellular carcinoma (HCC). Most lncRNAs deregulated in infected cells that have been described function to potentiate or block the antiviral response and, therefore, they have a great impact on HCV viral replication. In addition, several lncRNAs upregulated by the infection contribute to viral release. Finally, many lncRNAs have been described as deregulated in HCV-related HCC that function to enhance cell survival, proliferation, and tumor progression by different mechanisms. Interestingly, some HCV-related HCC lncRNAs can be detected in bodily fluids, and there is great hope that they could be used as biomarkers to predict cancer initiation, progression, tumor burden, response to treatment, resistance to therapy, or tumor recurrence. Finally, there is high confidence that lncRNAs could also be used to improve the suboptimal long-term outcomes of current HCC treatment options.
  • Autores: Unfried Huertas, Juan Pablo; Fortes, Puri (Autor de correspondencia)
    Revista: JOURNAL OF HEPATOLOGY (ONLINE)
    ISSN: 0168-8278 Vol.73 N° 5 2020 págs. 1010-1012
  • Autores: Valencia Leoz, Karmele; Erice, O.; Kostyrko, K.; et al.
    Revista: JOURNAL OF CLINICAL INVESTIGATION
    ISSN: 0021-9738 Vol.130 N° 4 2020 págs. 1879 - 1895
    Resumen
    Few therapies are currently available for patients with KRAS-driven cancers, highlighting the need to identify new molecular targets that modulate central downstream effector pathways. Here we found the miRNA cluster mir181ab1 as a key modulator of KRAS-driven oncogenesis. Ablation of Mir181ab1 in genetically-engineered mouse models of Kras-driven lung and pancreatic cancer was deleterious to tumor initiation and progression. Expression of both resident miRNAs in the Mir181ab1 cluster, miR181a1 and miR181b1, was necessary to rescue the Mir181ab1-loss phenotype underscoring their non-redundant role. In human cancer cells, depletion of miR181ab1 impaired proliferation and 3D growth, whereas overexpression provided a proliferative advantage. Lastly, we unveiled miR181ab1-regulated genes responsible for this phenotype. These studies identified what we believe to be a previously unknown role for miR181ab1 as a potential therapeutic target in two highly aggressive and difficult to treat KRAS-mutated cancers.
  • Autores: Enguita Germán, Mónica; Razquin Erro, Nerea; Pamplona, R.; et al.
    Revista: CELL DEATH AND DISEASE
    ISSN: 2041-4889 Vol.10 N° 1 2019 págs. 14
    Resumen
    Liver cirrhosis results from chronic hepatic damage and is characterized by derangement of the organ architecture with increased liver fibrogenesis and defective hepatocellular function. It frequently evolves into progressive hepatic insufficiency associated with high mortality unless liver transplantation is performed. We have hypothesized that the deficiency of critical nutrients such as essential omega-3 fatty acids might play a role in the progression of liver cirrhosis. Here we evaluated by LC-MS/MS the liver content of omega-3 docosahexaenoic fatty acid (DHA) in cirrhotic patients and investigated the effect of DHA in a murine model of liver injury and in the response of hepatic stellate cells (HSCs) (the main producers of collagen in the liver) to pro-fibrogenic stimuli. We found that cirrhotic livers exhibit a marked depletion of DHA and that this alteration correlates with the progression of the disease. Administration of DHA exerts potent anti-fibrogenic effects in an acute model of liver damage. Studies with HSCs show that DHA inhibits fibrogenesis more intensely than other omega-3 fatty acids. Data from expression arrays revealed that DHA blocks TGF beta and NF-kappa B pathways. Mechanistically, DHA decreases late, but not early, SMAD3 nuclear accumulation and inhibits p65/RelA-S536 phosphorylation, which is required for HSC survival. Notably, DHA increases ADRP expression, leading to the formation of typical quiescence-associated perinuclear lipid droplets. In conclusion, a marked depletion of DHA is present in the liver of patients with advanced cirrhosis. DHA displays anti-fibrogenic activities on HSCs targeting NF-kappa B and TGF beta pathways and inducing ADPR expression and quiescence in these cells.
  • Autores: Unfried Huertas, Juan Pablo; Serrano, G.; Suarez Alvarez, Beatriz; et al.
    Revista: CANCER RESEARCH
    ISSN: 0008-5472 Vol.79 N° 20 2019 págs. 5167 - 5180
    Resumen
    The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) datasets allow unprecedented gene expression analyses. Here, using these datasets, we performed pan-cancer and pan-tissue identification of coding and long noncoding RNA (lncRNA) transcripts differentially expressed in tumors and preferentially expressed in healthy tissues and/or tumors. Pan-cancer comparison of mRNAs and lncRNAs showed that lncRNAs were deregulated in a more tumor-specific manner. Given that lncRNAs are more tissue-specific than mRNAs, we identified healthy tissues that preferentially express lncRNAs upregulated in tumors and found that testis, brain, the digestive tract, and blood/spleen were the most prevalent. In addition, specific tumors also upregulate lncRNAs preferentially expressed in other tissues, generating a unique signature for each tumor type. Most tumors studied downregulated lncRNAs preferentially expressed in their tissue of origin, probably as a result of dedifferentiation. However, the same lncRNAs could be upregulated in other tumors, resulting in "bimorphic" transcripts. In hepatocellular carcinoma (HCC), the upregulated genes identified were expressed at higher levels in patients with worse prognosis. Some lncRNAs upregulated in HCC and preferentially expressed in healthy testis or brain were predicted to function as oncogenes and were significantly associated with higher tumor burden, and poor prognosis, suggesting their relevance in hepatocarcinogenesis and/or tumor evolution. Taken together, therapies targeting oncogenic lncRNAs should take into consideration the healthy tissue, where the lncRNAs are preferentially expressed, to predict and decrease unwanted secondary effects and increase potency. Significance: Comprehensive analysis of coding and noncoding genes expressed in different tumors and normal tissues, which should be taken into account to predict side effects from potential coding and noncoding gene-targeting therapies.
  • Autores: Valadkhan, S. (Autor de correspondencia); Fortes, Puri
    Revista: FRONTIERS IN MICROBIOLOGY
    ISSN: 1664-302X Vol.9 2018
    Resumen
    The interferon (IFN) response is a critical component of the innate immunity antiviral pathways in mammalians. IFN signaling results in increased expression of cellular factors that block key steps in the viral replication cycle. Many IFN-induced antiviral factors act through decreasing viral entry, replication, transcription, translation, packaging and release. However, these effects are also deleterious for the viability of the cell, which necessitates a tight control over the magnitude and duration of the IFN response. This is partially achieved through the IFN-mediated activation of negative regulatory factors that help in termination of the IFN response and return to a normal homeostatic state. Such built-in negative regulatory mechanisms are frequently hijacked by viruses such as the Hepatitis C virus (HCV) to increase viral replication and productive infections. We and others have shown that long non-coding RNAs (lncRNAs) play prominent roles in regulation of the IFN response. Activation of the IFN cascade alters the expression of a large number of lncRNAs, many of which are directly induced by the JAK/STAT pathway and thus, resemble the well-studied protein-coding interferon-stimulated genes (ISGs). While only a handful of IFN- and virally induced lncRNAs have been characterized, recent studies have identified several lncRNAs that act as positive or negative regulators of expression of ISGs during the IFN response. A number of such regulatory lncRNAs have multiple ISG targets, while others act on a single neighboring ISG. Another group of studied lncRNAs act further upstream and regulate the expression of IFN genes or factors that sense the presence of viral genome or replication products. The large number of unstudied IFN- and virally induced lncRNAs makes it highly likely that future studies will reveal a much greater share for this class of transcripts in regulation of the antiviral response. In addition to their physiological roles, the expression of such lncRNAs is frequently modulated by virally encoded factors to interfere with the antiviral response and promote viral replication, thus making them ideal targets for therapeutic intervention.
  • Autores: Fortes, Puri; Barriocanal Urbina, Marina
    Revista: NON-CODING RNA INVESTIGATION
    ISSN: 2522-6673 Vol.2 N° 2 2018

Proyectos desde 2018

  • Título: Alianza en Genómica Avanzada para el desarrollo de Terapias Personalizadas en Navarra
    Código de expediente: 0011-1411-2020-000010
    Investigador principal: FELIPE LUIS PROSPER CARDOSO, FELIPE LUIS PROSPER CARDOSO.
    Financiador: GOBIERNO DE NAVARRA
    Convocatoria: FIMA 2020 GN PROYECTOS ESTRATEGICOS DE I+D 2020-2022
    Fecha de inicio: 17-06-2020
    Fecha fin: 30-11-2022
    Importe concedido: 725.480,08€
    Otros fondos: -
  • Título: Inhibición de genes no codificantes con valor terapéutico en hepatocarcinoma. Análisis de monoterapias y terapias combinadas.
    Código de expediente: PI19/00742
    Investigador principal: BRUNO CARLOS SANGRO GOMEZ-ACEBO, BRUNO CARLOS SANGRO GOMEZ-ACEBO.
    Financiador: INSTITUTO DE SALUD CARLOS III
    Convocatoria: 2019 AES Proyectos de investigación
    Fecha de inicio: 01-01-2020
    Fecha fin: 31-12-2023
    Importe concedido: 93.170,00€
    Otros fondos: Fondos FEDER
  • Título: Análisis de RNAs largos no codificantes relacionados con supervivencia que permiten el crecimiento del carcinoma hepatocelular
    Código de expediente: RTI2018-101759-B-I00
    Investigador principal: MARIA PURIFICACION FORTES ALONSO.
    Financiador: MINISTERIO DE CIENCIA E INNOVACIÓN
    Convocatoria: 2018 - PROYECTOS DE I+D RETOS INVESTIGACION
    Fecha de inicio: 01-01-2019
    Fecha fin: 30-09-2022
    Importe concedido: 133.100,00€
    Otros fondos: Fondos FEDER
  • Título: Desarrollo de secuencias de RNA para regular genes terapéuticos.
    Código de expediente: 0011-1383-2019-000006
    Investigador principal: MARIA PURIFICACION FORTES ALONSO, MARIA PURIFICACION FORTES ALONSO.
    Financiador: GOBIERNO DE NAVARRA
    Convocatoria: 2019 - GN INDUSTRIA PROYECTOS CENTROS TECNOLOGICOS Y ORGANISMOS DE INVESTIGACION
    Fecha de inicio: 01-12-2018
    Fecha fin: 30-11-2019
    Importe concedido: 132.647,50€
    Otros fondos: -
  • Título: TERegNA. Desarrollo de secuencias de RNA para regular genes terapéuticos
    Código de expediente: 0011-1383-2018-000011
    Investigador principal: MARIA PURIFICACION FORTES ALONSO.
    Financiador: GOBIERNO DE NAVARRA
    Convocatoria: 2018 - GN INDUSTRIA PROYECTOS CENTROS TECNOLOGICOS Y ORGANISMOS DE INVESTIGACION
    Fecha de inicio: 01-02-2018
    Fecha fin: 30-11-2018
    Importe concedido: 145.028,60€
    Otros fondos: -
  • Título: Desarrollo de nuevos fármacos para el tratamiento del hepatocarcinoma
    Código de expediente: 0011-1408-2017-000008
    Investigador principal: BEATRIZ SUAREZ ALVAREZ.
    Financiador: GOBIERNO DE NAVARRA
    Convocatoria: 2017 -GN DOCTORANDOS INDUSTRIALES 2018- 2020
    Fecha de inicio: 26-09-2017
    Fecha fin: 25-09-2020
    Importe concedido: 90.000,00€
    Otros fondos: -
  • Título: Desarrollo terapéutico basado en la identificación, análisis e inhibición de genes no codificantes implicados en la progresión del hepatocarcinoma.
    Código de expediente: PI16/01845
    Investigador principal: BRUNO CARLOS SANGRO GOMEZ-ACEBO, BRUNO CARLOS SANGRO GOMEZ-ACEBO.
    Financiador: INSTITUTO DE SALUD CARLOS III
    Convocatoria: 2016 AES PROYECTOS DE INVESTIGACIÓN
    Fecha de inicio: 01-01-2017
    Fecha fin: 31-12-2019
    Importe concedido: 163.652,50€
    Otros fondos: Fondos FEDER
  • Título: Estudio de la acción antifibrogénica de los ácidos grasos omega 3 : Aplicaciones terapéuticas
    Código de expediente: PI16/02081
    Investigador principal: JORGE AUGUSTO QUIROGA VILA, JORGE AUGUSTO QUIROGA VILA.
    Financiador: INSTITUTO DE SALUD CARLOS III
    Convocatoria: 2016 AES PROYECTOS DE INVESTIGACIÓN
    Fecha de inicio: 01-01-2017
    Fecha fin: 30-06-2021
    Importe concedido: 139.755,00€
    Otros fondos: Fondos FEDER
  • Título: Nuevo tratamiento para pacientes con fibrosis hepática. Evaluación de la eficacia clínica
    Código de expediente: 0011-1365-2016-000308
    Investigador principal: MARIA PURIFICACION FORTES ALONSO, MARIA PURIFICACION FORTES ALONSO.
    Financiador: GOBIERNO DE NAVARRA
    Convocatoria: 2016 - GN PROYECTOS TRACTORES DE CENTROS TECNOLOGICOS (ADITECH)
    Fecha de inicio: 01-07-2016
    Fecha fin: 31-08-2018
    Importe concedido: 104.289,00€
    Otros fondos: -
  • Título: Análisis de RNAs largos no codificantes asociados a hepatocarcinoma y evaluación de su potencial como dianas terapéuticas
    Código de expediente: SAF2015-70971-R
    Investigador principal: MARIA PURIFICACION FORTES ALONSO, MARIA PURIFICACION FORTES ALONSO.
    Financiador: MINISTERIO DE CIENCIA E INNOVACIÓN
    Convocatoria: 2015 - PROYECTOS DE I+D RETOS
    Fecha de inicio: 01-01-2016
    Fecha fin: 31-03-2019
    Importe concedido: 116.800,00€
    Otros fondos: Fondos FEDER
  • Título: Desarrollo de compuestos terapéuticos para el bloqueo de RNA largos no codificantes implicados en cirrosis hepática y hepatocarcinoma identificados mediante análisis bioinformático y molecular
    Código de expediente: 33/2015
    Investigador principal: VICTORIANO SEGURA RUIZ, VICTORIANO SEGURA RUIZ.
    Financiador: GOBIERNO DE NAVARRA. DEPARTAMENTO DE SALUD
    Convocatoria: 2015 PROYECTOS DE I+D EN SALUD
    Fecha de inicio: 06-12-2015
    Fecha fin: 05-12-2018
    Importe concedido: 49.627,00€
    Otros fondos: Fondos FEDER
  • Título: De transcritos del testículo a nuevas terapias contra el cáncer
    Investigador principal: MARIA PURIFICACION FORTES ALONSO
    Financiador: ASOCIACION ESPAÑOLA CONTRA EL CANCER
    Convocatoria: FIMA Ideas Semilla 2020
    Fecha de inicio: 01-09-2020
    Fecha fin: 31-10-2022
    Importe concedido: 20.000,00€
  • Título: "Desarrollo de nuevos tratamientos para la fibrosis hepática" ACUERDO UNICAJA 2017 PFA
    Investigador principal: MARIA PURIFICACION FORTES ALONSO
    Financiador: FUNDACION BANCARIA UNICAJA
    Convocatoria:
    Fecha de inicio: 24-03-2017
    Fecha fin: 31-12-2025
    Importe concedido: 25.000,00€