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  1. Article ; Online: S-Nitrosylation at the intersection of metabolism and autophagy: Implications for cancer.

    Guil-Luna, Silvia / Sanchez-Montero, María Teresa / Rodríguez-Ariza, Antonio

    Biochimica et biophysica acta. Reviews on cancer

    2023  Volume 1878, Issue 6, Page(s) 189012

    Abstract: Metabolic plasticity, which determines tumour growth and metastasis, is now understood to be a flexible and context-specific process in cancer metabolism. One of the major pathways contributing to metabolic adaptations in eucaryotic cells is autophagy, a ...

    Abstract Metabolic plasticity, which determines tumour growth and metastasis, is now understood to be a flexible and context-specific process in cancer metabolism. One of the major pathways contributing to metabolic adaptations in eucaryotic cells is autophagy, a cellular degradation and recycling process that is activated during periods of starvation or stress to maintain metabolite and biosynthetic intermediate levels. Consequently, there is a close association between the metabolic adaptive capacity of tumour cells and autophagy-related pathways in cancer. Additionally, nitric oxide regulates protein function and signalling through S-nitrosylation, a post-translational modification that can also impact metabolism and autophagy. The primary objective of this review is to provide an up-to-date overview of the role of S-nitrosylation at the intersection of metabolism and autophagy in cancer. First, we will outline the involvement of S-nitrosylation in the metabolic adaptations that occur in tumours. Then, we will discuss the multifaceted role of autophagy in cancer, the interplay between metabolism and autophagy during tumour progression, and the contribution of S-nitrosylation to autophagic dysregulation in cancer. Finally, we will present insights into relevant therapeutic aspects and discuss prospects for the future.
    MeSH term(s) Humans ; Nitric Oxide ; Autophagy ; Protein Processing, Post-Translational ; Signal Transduction ; Neoplasms/pathology
    Chemical Substances Nitric Oxide (31C4KY9ESH)
    Language English
    Publishing date 2023-10-31
    Publishing country Netherlands
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2918802-7
    ISSN 1879-2561 ; 0304-419X
    ISSN (online) 1879-2561
    ISSN 0304-419X
    DOI 10.1016/j.bbcan.2023.189012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Galectin-3 depletion tames pro-tumoural microglia and restrains cancer cells growth.

    Rivera-Ramos, Alberto / Cruz-Hernández, Luis / Talaverón, Rocío / Sánchez-Montero, María Teresa / García-Revilla, Juan / Mulero-Acevedo, Marta / Deierborg, Tomas / Venero, José Luis / Sarmiento Soto, Manuel

    Cancer letters

    2024  Volume 591, Page(s) 216879

    Abstract: Galectin-3 (Gal-3) is a multifunctional protein that plays a pivotal role in the initiation and progression of various central nervous system diseases, including cancer. Although the involvement of Gal-3 in tumour progression, resistance to treatment and ...

    Abstract Galectin-3 (Gal-3) is a multifunctional protein that plays a pivotal role in the initiation and progression of various central nervous system diseases, including cancer. Although the involvement of Gal-3 in tumour progression, resistance to treatment and immunosuppression has long been studied in different cancer types, mainly outside the central nervous system, its elevated expression in myeloid and glial cells underscores its profound impact on the brain's immune response. In this context, microglia and infiltrating macrophages, the predominant non-cancerous cells within the tumour microenvironment, play critical roles in establishing an immunosuppressive milieu in diverse brain tumours. Through the utilisation of primary cell cultures and immortalised microglial cell lines, we have elucidated the central role of Gal-3 in promoting cancer cell migration, invasion, and an immunosuppressive microglial phenotypic activation. Furthermore, employing two distinct in vivo models encompassing primary (glioblastoma) and secondary brain tumours (breast cancer brain metastasis), our histological and transcriptomic analysis show that Gal-3 depletion triggers a robust pro-inflammatory response within the tumour microenvironment, notably based on interferon-related pathways. Interestingly, this response is prominently observed in tumour-associated microglia and macrophages (TAMs), resulting in the suppression of cancer cells growth.
    MeSH term(s) Microglia/metabolism ; Microglia/pathology ; Galectin 3/metabolism ; Galectin 3/genetics ; Humans ; Tumor Microenvironment ; Animals ; Glioblastoma/pathology ; Glioblastoma/metabolism ; Glioblastoma/genetics ; Glioblastoma/immunology ; Brain Neoplasms/pathology ; Brain Neoplasms/metabolism ; Brain Neoplasms/genetics ; Brain Neoplasms/immunology ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Female ; Breast Neoplasms/pathology ; Breast Neoplasms/metabolism ; Breast Neoplasms/genetics ; Breast Neoplasms/immunology ; Tumor-Associated Macrophages/metabolism ; Tumor-Associated Macrophages/immunology ; Macrophages/metabolism ; Macrophages/immunology ; Neoplasm Invasiveness ; Blood Proteins/metabolism ; Galectins/metabolism ; Galectins/genetics ; Signal Transduction ; Mice ; Gene Expression Regulation, Neoplastic
    Language English
    Publishing date 2024-04-16
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2024.216879
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    Zs.A 1177: Show issues Location:
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  3. Article ; Online: Clinical significance of glycogen synthase kinase 3 (GSK-3) expression and tumor budding grade in colorectal cancer: Implications for targeted therapy.

    Guil-Luna, Silvia / Rivas-Crespo, Aurora / Navarrete-Sirvent, Carmen / Mantrana, Ana / Pera, Alejandra / Mena-Osuna, Rafael / Toledano-Fonseca, Marta / García-Ortíz, María Victoria / Villar, Carlos / Sánchez-Montero, Maria Teresa / Krueger, Janna / Medina-Fernández, Francisco Javier / De La Haba-Rodríguez, Juan / Gómez-España, Auxiliadora / Aranda, Enrique / Rudd, Christopher E / Rodríguez-Ariza, Antonio

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    2023  Volume 167, Page(s) 115592

    Abstract: Introduction: Glycogen synthase kinase 3 (GSK-3) has been proposed as a novel cancer target due to its regulating role in both tumor and immune cells. However, the connection between GSK-3 and immunoevasive contexture, including tumor budding (TB) has ... ...

    Abstract Introduction: Glycogen synthase kinase 3 (GSK-3) has been proposed as a novel cancer target due to its regulating role in both tumor and immune cells. However, the connection between GSK-3 and immunoevasive contexture, including tumor budding (TB) has not been previously examined.
    Methods: we investigated the expression levels of total GSK-3 as well as its isoforms (GSK-3β and GSK-3α) and examined their potential correlation with TB grade and the programmed cell death-ligand 1 (PD-L1) in colorectal cancer (CRC) tumor samples. Additionally, we compared the efficacy of GSK-3-inhibition with PD-1/PD-L1 blockade in humanized patient-derived (PDXs) xenografts models of high-grade TB CRC.
    Results: we show that high-grade (BD3) TB CRC is associated with elevated expression levels of total GSK-3, specifically the GSK-3β isoform, along with increased expression of PD-L1 in tumor cells. Moreover, we define an improved risk stratification of CRC patients based on the presence of GSK-3
    Conclusions: our study provides compelling evidence for the clinical significance of GSK-3 expression and TB grade in risk stratification of CRC patients. Moreover, our findings strongly support GSK-3 inhibition as an effective therapy specifically targeting high-grade TB in CRC.
    MeSH term(s) Humans ; CD8-Positive T-Lymphocytes ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinase 3 beta ; B7-H1 Antigen ; Programmed Cell Death 1 Receptor ; Clinical Relevance ; Colorectal Neoplasms/pathology
    Chemical Substances Glycogen Synthase Kinase 3 (EC 2.7.11.26) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; B7-H1 Antigen ; Programmed Cell Death 1 Receptor
    Language English
    Publishing date 2023-09-29
    Publishing country France
    Document type Journal Article
    ZDB-ID 392415-4
    ISSN 1950-6007 ; 0753-3322 ; 0300-0893
    ISSN (online) 1950-6007
    ISSN 0753-3322 ; 0300-0893
    DOI 10.1016/j.biopha.2023.115592
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Metabolic shift underlies tumor progression and immune evasion in S-nitrosoglutathione reductase-deficient cancer.

    Mena-Osuna, Rafael / Mantrana, Ana / Guil-Luna, Silvia / Sánchez-Montero, María Teresa / Navarrete-Sirvent, Carmen / Morales-Ruiz, Teresa / Rivas-Crespo, Aurora / Toledano-Fonseca, Marta / García-Ortíz, María Victoria / García-Jurado, Gema / Gómez-España, María Auxiliadora / González-Fernández, Rafael / Villar, Carlos / Medina-Fernández, Francisco Javier / Villalba, José Manuel / Aranda, Enrique / Rodríguez-Ariza, Antonio

    The Journal of pathology

    2023  Volume 260, Issue 3, Page(s) 261–275

    Abstract: S-nitrosoglutathione reductase (GSNOR) is a denitrosylase enzyme that has been suggested to play a tumor suppressor role, although the mechanisms responsible are still largely unclear. In this study, we show that GSNOR deficiency in tumors is associated ... ...

    Abstract S-nitrosoglutathione reductase (GSNOR) is a denitrosylase enzyme that has been suggested to play a tumor suppressor role, although the mechanisms responsible are still largely unclear. In this study, we show that GSNOR deficiency in tumors is associated with poor prognostic histopathological features and poor survival in patients with colorectal cancer (CRC). GSNOR-low tumors were characterized by an immunosuppressive microenvironment with exclusion of cytotoxic CD8
    MeSH term(s) Mice ; Animals ; Humans ; Oxidoreductases ; CD8-Positive T-Lymphocytes ; Immune Evasion ; Proteomics ; Neoplasms ; Tumor Microenvironment
    Chemical Substances Oxidoreductases (EC 1.-) ; formaldehyde dehydrogenase, glutathione-independent (EC 1.2.1.46)
    Language English
    Publishing date 2023-04-05
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3119-7
    ISSN 1096-9896 ; 0022-3417
    ISSN (online) 1096-9896
    ISSN 0022-3417
    DOI 10.1002/path.6080
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