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Targeting metabolism to improve immunotherapy in GSNOR-deficient colorectal cancer

ABSTRACT: Targeting metabolism to improve immunotherapy in GSNOR-deficient colorectal cancer

PROVIDER: PRJEB74194 | ENA |

REPOSITORIES: ENA

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Targeting metabolism to improve immunotherapy in GSNOR-deficient colorectal cancer

Project description:Targeting metabolism to improve immunotherapy in GSNOR-deficient colorectal cancer

| PRJEB74195 | ENA

Targeting metabolism to improve immunotherapy in GSNOR-deficient colorectal cancer

Project description:Targeting metabolism to improve immunotherapy in GSNOR-deficient colorectal cancer

| PRJNA1099593 | ENA

Targeting metabolism to improve immunotherapy in GSNOR-deficient colorectal cancer

Project description:Colorectal cancer (CRC) is the third most diagnosed type of cancer and the second leading cause of cancer death worldwide. Despite the increasing knowledge of CRC molecular biology and the development of new targeted therapies, its high heterogeneity hampers the efficacy of current treatments. Thus, there is a pressing need to identify new effective therapeutic targets and improve immune therapies for these patients. In this regard, S-nitrosoglutathione reductase (GSNOR) is a denitrosylase enzyme that has been suggested to play a tumour suppressor role, although the mechanisms responsible are still largely unclear. Therefore, the main objective of this project was to understand the role of GSNOR in CRC tumorigenesis and its therapeutic implications. Firstly, we classified CRC tumours as GSNOR-high or low according to their GSNOR expression as assessed by immunohistochemistry (IHC). Accordingly, we found that GSNOR deficiency was associated with worse prognosis factors such as a larger tumour size at diagnosis, higher TNM stage, higher grade of tumour budding (TB), the CMS4 subtype, lower expression of the intestinal differentiation markers CDX2 and AE1/AE3 cytokeratin and a worse progression free survival (PFS) and overall survival (OS). We next investigated the differences in gene expression between CRC GSNOR-high and low tumours, uncovering significant alterations in metabolism and immune system pathways. Hence, GSNOR-deficient tumours were characterized by immune suppressive features and a dysregulation of their metabolism, favouring other metabolic pathways than OXPHOS.

2024-04-13 | GSE263844 | GEO

Immune gene signatures in human colorectal tumors with different GSNOR/ADH5 expression

Project description:The study was designed to explore the relationships between GSNOR/ADH5 expression and the tumor immune microenvironment

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S-nitrosoglutathione reductase GSNOR drives age-related obesity by promoting adipose tissue whitening through de-nitrosation of Beclin-1

Project description:Age-related obesity is a growing public health concern linked to various metabolic disorders, yet its underlying mechanisms remain incompletely understood. Here we report that S-nitrosoglutathione reductase (GSNOR), a pivotal denitrosation enzyme, increases in adipose tissue of both male mice and humans from middle-age. GSNOR knockout protects against age-related weight gain and enhances metabolism, whereas adipose-specific GSNOR knock-in mice promotes obesity and metabolic decline. Further investigation reveals that aged GSNOR KO mice maintain higher mitochondrial content and more beige adipocytes, whereas adipose-specific GSNOR overexpression promotes adipose tissue whitening. Mechanistically, GSNOR denitrosates Beclin-1 at cysteine 351 and mutation of this site (Beclin-1C351A) increases autophagy by enhancing Beclin-1 and ATG14 interaction, thereby accelerating beige-to-white adipocyte conversion. Together, our findings reveal that GSNOR regulates adipose tissue remodeling during aging through Beclin-1 S-nitrosation, pointing to a potential therapeutic target for age-related obesity.

2026-01-26 | GSE317377 | GEO

Fes-Deficient Macrophages Prime CD8+ T Cells to Stimulate Anti-tumor Immunity and Improve Immunotherapy Efficacy

Project description:Fes-Deficient Macrophages Prime CD8+ T Cells to Stimulate Anti-tumor Immunity and Improve Immunotherapy Efficacy

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Fes-Deficient Macrophages Prime CD8+ T Cells to Stimulate Anti-tumor Immunity and Improve Immunotherapy Efficacy

Project description:Homeostatic immunoregulatory mechanisms that prevent adverse effects of immune overaction can serve as barriers to successful anti-cancer immunity, representing attractive targets to improve cancer immunotherapy. Here, we demonstrated the role of the non-receptor tyrosine kinase Fes, abundantly expressed in immune cells, as an innate intracellular immune checkpoint. Host Fes-deficiency delayed tumor onset in a gene dose-dependent manner and improved tumor control, survival, doxorubicin efficacy, and anti-PD-1 therapy sensitization in murine triple-negative breast cancer and melanoma models. These effects were associated with a shift to an anti-tumorigenic immune microenvironment. Fes-deficient macrophages displayed increased Toll-like receptor signaling, proinflammatory cytokine production, antigen presentation to and activation of T cells, leading to increased cancer cell killing in vitro and tumor control in vivo. This study highlights Fes as an innate immune checkpoint with potential as a therapeutic target and a predictive biomarker to guide immune checkpoint inhibitor treatment.

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Targeting METTL3 reprograms tumor microenvironment to improve cancer immunotherapy [RNA-seq]

Project description:Targeting METTL3 reprograms tumor microenvironment to improve cancer immunotherapy [RNA-seq]

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Targeting Arachidonic Acid Metabolism Enhances Immunotherapy Efficacy in ARID1A-Deficient Colorectal Cancer.

Project description: Not available

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DNA barcoding reveals ongoing immunoediting of clonal cancer populations during metastatic progression and in response to immunotherapy

Project description:Cancers evade the immune system in order to grow or metastasise through the process of cancer immunoediting. While checkpoint inhibitor therapy has been effective for reactivating tumour immunity in some cancers, many solid cancers, including breast cancer, remain largely non-responsive. Understanding the way non-responsive cancers evolve to evade immunity, what resistance pathways are activated and whether this occurs at the clonal level will improve immunotherapeutic design. We tracked cancer cell clones during the immunoediting process and determined clonal transcriptional profiles that allow immune evasion in murine mammary tumour growth in response to immunotherapy with anti-PD1 and anti-CTLA4. Clonal diversity was significantly restricted by immunotherapy treatment at both the primary and metastatic sites. These findings demonstrate that immunoediting selects for pre-existing breast cancer cell populations, that immunoediting is not a static process and is ongoing during metastasis and immunotherapy treatment. Isolation of immunotherapy resistant clones revealed unique and overlapping transcriptional signatures. The overlapping gene signature was predictive of poor survival in basal-like breast cancer patient cohorts. Some of these overlapping genes have existing small molecules which can be used to potentially improve immunotherapy response.

2021-09-01 | E-MTAB-10027 | biostudies-arrayexpress

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