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RNA-sequencing on sorted infiltrating CD8 T cells from vehicle or JHU083, pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treated MC38 (colon cancer) tumor bearing mice

ABSTRACT: RNA-sequencing on sorted infiltrating CD8 T cells from vehicle or JHU083, pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treated MC38 (colon cancer) tumor bearing mice

PROVIDER: PRJNA492801 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7892580.fastq.gz	Fastqsanger.gz
	SRR7892581.fastq.gz	Fastqsanger.gz
	SRR7892582.fastq.gz	Fastqsanger.gz
	SRR7892583.fastq.gz	Fastqsanger.gz
	SRR7892584.fastq.gz	Fastqsanger.gz

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RNA-sequencing on sorted infiltrating CD8 T cells from vehicle or JHU083, pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treated MC38 (colon cancer) tumor bearing mice

Project description:RNA-sequencing was performed on sorted CD11b-CD11c-B220-CD45+TCRbeta+CD44+CD8+ TIL from vehicle or JHU083 treated MC38 tumor-bearing mice with or without JHU083, pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treatment for expression profiling

2020-02-24 | GSE120345 | GEO

RNA-sequencing on sorted tumor-associated macrophages from vehicle or JHU083 pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treated 4T1 (breast cancer) tumor bearing mice

Project description:RNA-sequencing was performed on sorted tumor-associated macrophages (CD45+7AAD-CD11b+F4/80+CD8-Ly6C-Ly6G-) from 4T1 tumor (murine breast cancer) bearig mice with or without JHU083, pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treatment for expression profiling

2020-07-08 | GSE119733 | GEO

Glutamine antagonist JHU083 reprograms immunosuppressive tumor-associated macrophages to drive tumor immunity in urologic cancers, bulk RNA-seq

Project description:Glutamine metabolism in the tumor microenvironment is emerging as a critical regulator of immune-mediated anti-tumor responses. We report potent tumor growth inhibition by the glutamine antagonist prodrug JHU083 in urologic tumors by JHU083-reprogrammed tumor-associated macrophages (TAMs) and tumor-infiltrating monocytes (TIMs). Using orthogonal approaches, we show that JHU083-mediated glutamine antagonism in the tumor microenvironment induces TNF, inflammatory, and mTORC1 signaling in different intra-tumoral TAM clusters. Additionally, we report that JHU083 increases proliferation in tissue-resident macrophages intratumorally and in different TAM sub-clusters. Functionally, we report that JHU083-reprogrammed TAMs have increased tumor cell phagocytosis and diminished pro-angiogenic capacities. In vivo inhibition of glutamine consumption in TAMs results in increased glycolysis, broken TCA cycle, and disruption in purine metabolism. Although the effect of glutamine antagonism was less profound on tumor-infiltrating T cells for their anti-tumor activity, it promoted a stem cell-like phenotype in CD8+ T cells and decreased the CD4+ Treg abundance. Additionally, we report that JHU083 causes a global shutdown in glutamine utilizing metabolic pathways in tumor cells, leading to reduced HIF-1, c-MYC phosphorylation, and induction of tumor cell apoptosis, all key anti-tumoral features.

2024-05-18 | GSE229222 | GEO

Glutamine antagonist JHU083 reprograms immunosuppressive tumor-associated macrophages to drive tumor immunity in urologic cancers, single-cell RNA-seq

2024-05-18 | GSE229223 | GEO

Glutamine antagonist JHU083 reprograms immunosuppressive tumor-associated macrophages to drive tumor immunity in urologic cancer

Project description:Glutamine antagonist JHU083 reprograms immunosuppressive tumor-associated macrophages to drive tumor immunity in urologic cancer

| PRJNA957765 | ENA

Combined with Gefitinib Overcomes Immunosuppression Induced by long-term Glutamine blockade in Bladder Cancer

Project description:Glutamine is a major energy source for tumor cells and blocking glutamine metabolism is being investigated as a promising strategy for cancer therapy. However, the antitumor effect of glutamine blockade in bladder cancer remains unclear, necessitating further investigation. Here, we demonstrated that glutamine metabolism was involved in the malignant progression of bladder cancer. Treatment with the glutamine antagonist 6-Diazo-5-oxo-L-norleucine (DON) inhibited bladder cancer cells in vitro in several ways. In addition, we observed a remarkable inhibition of tumor growth in bladder cancer-bearing mice using JHU083, a prodrug that was designed to prevent DON-induced toxicity. However, the antitumor immune effect of T cells changed from activation to inhibition as the administrated time extended. We found that both in vitro treatment with DON and in vivo prolonged administration of JHU083 led to the upregulation of PD-L1 in bladder cancer cells. Mechanistically, glutamine blockade up-regulates PD-L1 expression in bladder cancer cells by accumulating ROS, subsequently activating the EGFR/ERK/C-Jun signaling pathway. Combinatorial treatment with JHU083 and gefitinib reversed the up-regulation of PD-L1 in bladder cancer cells induced by prolonged glutamine blockade. This reversal resulted in the alleviation of T-cell immunosuppression and a significant improvement in therapeutic outcome. These preclinical findings suggested that broad targeting of glutamine metabolism could represent a viable therapeutic strategy for bladder cancer, with the potential for further enhancement through combined treatment with gefitinib.

2024-08-08 | GSE269520 | GEO

Glutamine antagonist JHU083 reprograms immunosuppressive tumor-associated macrophages to drive tumor immunity in urologic cancers, bulk RNA-seq

Project description:Glutamine antagonist JHU083 reprograms immunosuppressive tumor-associated macrophages to drive tumor immunity in urologic cancers, bulk RNA-seq

| PRJNA953423 | ENA

RNA-sequencing on sorted tumor-associated macrophages from vehicle or JHU083 pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treated 4T1 (breast cancer) tumor bearing mice

Project description:RNA-sequencing on sorted tumor-associated macrophages from vehicle or JHU083 pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treated 4T1 (breast cancer) tumor bearing mice

| PRJNA490152 | ENA

Glutamine antagonist JHU083 reprograms immunosuppressive tumor-associated macrophages to drive tumor immunity in urologic cancers, single-cell RNA-seq

Project description:Glutamine antagonist JHU083 reprograms immunosuppressive tumor-associated macrophages to drive tumor immunity in urologic cancers, single-cell RNA-seq

| PRJNA953426 | ENA

Microbial Bile acid metabolite, 3-oxo-LCA, prohibits colorectal cancer progression

Project description:Objective: Bile acids (BAs) not only influence gut microbiome composition but are also metabolized by gut bacteria to form various microbial BAs. Among these, 3-oxo-lithocholic acid (-oxo-LCA) and isoalloLCA have been reported to modulate host immunity, suppress intestinal pathogens, and provide anti-aging benefits. However, their specific effects on intestinal epithelial cells (IECs) and their role in colorectal cancer (CRC) progression remain unclear. Design: To investigate the impact of 3-oxo-LCA on intestinal tumorigenesis, we examined its effects on the growth of mouse and human CRC cell lines (CT26, MC38, HCT116), as well as on primary mouse intestinal organoids and patient-derived CRC organoids (PDCOs). Additionally, we evaluated its role in vivo using APCMin/+ mice and multiple CRC models, including syngeneic CT26 and MC38 models, as well as HCT116 and PDX-derived xenografts in NSG (immunodeficient) mice. Results: Our findings show that 3-oxo-LCA is a potent FXR agonist that restores FXR signaling both in vitro and in vivo. This results in reduced growth of CRC cell lines and suppression of intestinal stem cell (ISC)’s proliferation in both mouse organoids and PDCOs. In APCMin/+ mice, 3-oxo-LCA reduced BA levels, enhanced gut barrier function, decreased tumor burden, and blocked tumor initiation. Furthermore, it significantly inhibited tumor progression in syngeneic and xenograft mouse models and promoted apoptosis within the tumors, enhancing cancer cell death. Conclusion: These results underscore the therapeutic potential of 3-oxo-LCA as a novel FXR agonist for CRC treatment, with its ability to inhibit tumorigenesis and progression by modulating epithelial cell proliferation and inducing apoptosis.

2025-08-14 | GSE294276 | GEO

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