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Immunosuppressive tumor microenvironment of osteosarcoma [scRNA-seq]

ABSTRACT: Immunosuppressive tumor microenvironment of osteosarcoma [scRNA-seq]

PROVIDER: PRJNA1272125 | ENA |

REPOSITORIES: ENA

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Immunosuppressive tumor microenvironment of osteosarcoma [scRNA-seq]

Project description:Osteosarcoma is the most common malignant bone tumor in children, characterized by a high degree of genomic instability, resulting in copy-number alterations and genomic rearrangements without disease-defining recurrent mutations. Clinical trials based on molecular characterization have failed to find new effective therapies or improve outcomes over the last 40 years. To better understand the immune microenvironment of osteosarcoma, we performed single-cell RNA sequencing on six tumor biopsy samples, combined with a previously-published cohort of six samples. Additional osteosarcoma samples were profiled using spatial transcriptomics for validation of discovered subtypes and to add spatial context. Analysis revealed immunosuppressive cells, including myeloid-derived suppressor cells (MDSCs), regulatory and exhausted T-cells, and LAMP3+ dendritic cells. Using cell-cell communication modeling, we identified robust interactions between MDSCs and other cells, leading to NF-κB upregulation and an immunosuppressive microenvironment, as well as interactions involving regulatory T-cells and osteosarcoma cells that promoted tumor progression and a proangiogenic niche.

2025-07-15 | GSE299023 | GEO

Immunosuppressive tumor microenvironment of osteosarcoma [Spatial transcriptomics]

Project description:Immunosuppressive tumor microenvironment of osteosarcoma [Spatial transcriptomics]

| PRJNA1272124 | ENA

Immunosuppressive tumor microenvironment of osteosarcoma [Spatial transcriptomics]

2025-07-15 | GSE299025 | GEO

Tumor-derived RAC1A159V mutation promotes an immunosuppressive tumor microenvironment that represses response to immune checkpoint inhibitor [scRNA-seq]

Project description:Immune checkpoint inhibitors that activate cytotoxic T lymphocytes to kill cancer cells have seen great success in therapies against various tumor types. However, the overall response rate in patients remains unacceptable at ~15%. RAC1, a member of Rho GTPase family, regulates multiple cellular processes in cancer, including vesicle trafficking, glycolysis, and exocytosis/endocytosis, which may contribute to tumor immune microenvironment modulation. RAC1A159V is a hotspot mutation found in several cancer types including colon cancer and is associated with poor prognosis. In this study, we have generated MC38 RAC1A159V cells by using CRISPR/Cas9 and confirmed that RAC1A159V results in upregulated RAC1 activity and downstream PAK1 and mTOR signaling. We have found the RAC1A159V tumors grow at a similar rate as RAC1WT tumors in immunodeficient NSG mice but faster than RAC1WT tumors in syngeneic immunoproficient mice, and the RAC1A159V tumors are highly resistant to anti-PD1 treatment. Flow cytometry and scRNA-seq analyses reveal that RAC1A159V cells form “cold” tumors with an immunosuppressive microenvironment and suppressed tumor-immune cell interactions. Mechanistically, we show RAC1A159V upregulates glycosphingolipid biosynthesis to activate mTORC1 signaling in tumor cells, which in turn increases glycolysis, impairs key chemokine production, and decreases IFNGR1 expression of the tumor cells. mTORC1 inhibition re-sensitizes the RAC1A159V tumors to anti-PD1 treatment by reversing effects by RAC1A159V mutation on tumor cell glycolysis, chemokine production, and IFNGR1 expression. Our results demonstrate that RAC1A159V in tumors drives immune evasion via mTOR mediated glycolysis, chemotaxis, and IFN-γ response, and further suggest an approach of combining targeting of RAC1-mTOR signaling with immune checkpoint inhibitors for the treatment of immune-cold RAC1A159V tumors.

2025-09-03 | GSE298274 | GEO

Single cell analysis of osteosarcoma tissues

Project description:We performed the scRNA-seq anakysis of 11 osteosarcoma tissues based on the 10X Genomics platform. The heterogneity of maglignant cells and the tumor microenvironment were analyzed.

2020-06-09 | GSE152048 | GEO

An oncolytic virus–delivered TGFβ inhibitor overcomes the immunosuppressive tumor microenvironment

Project description:An oncolytic virus–delivered TGFβ inhibitor overcomes the immunosuppressive tumor microenvironment

| PRJNA779090 | ENA

CD74 regulates the tumor immunosuppressive microenvironment in triple-negative brest cancer

Project description:CD74 regulates the tumor immunosuppressive microenvironment in triple-negative brest cancer

| PRJNA1070602 | ENA

Proteasome regulator PSME4 reduces cellular inflammation and promotes an immunosuppressive tumor microenvironment

Project description:Proteasome regulator PSME4 reduces cellular inflammation and promotes an immunosuppressive tumor microenvironment

| PRJEB53036 | ENA

Single cell sequencing reveals the immunosuppressive trajectory in the tumor microenvironment of human giant cell tumor of bone

Project description:GCTB is a type of bone tumor. we used scRNA-seq analysis to investigate the tumour microenvironment (TME) in GCTB.

2024-09-30 | GSE254672 | GEO

Tumor-initiating stem cell shapes its microenvironment into an immunosuppressive barrier and pro-tumorigenic niche

Project description:Tumor-initiating stem cells (TSCs) are critical for drug resistance and immune escape. However, the mutual regulations between TSC and tumor microenvironment (TME) remain unclear. Using DNA-label retaining, single-cell RNA sequencing (scRNA-seq), and other approaches, we investigated intestinal adenoma in response to chemoradiotherapy (CRT), thus identifying therapy-resistant TSCs (TrTSCs). We find bidirectional crosstalk between TSCs and TME using CellPhoneDB analysis. An intriguing finding is that TSCs shape TME into a landscape that favors TSCs for immunosuppression and propagation. Using adenoma-organoid co-cultures, niche-cell depletion, and lineaging tracing, we characterize a functional role of cyclooxygenase-2 (Cox-2)-dependent signaling, predominantly occurring between tumor-associated monocytes and macrophages (TAMMs) and TrTSCs. We show that TAMMs promote TrTSC proliferation through prostaglandin E2 (PGE2)-PTGER4(EP4) signaling, which enhances β-catenin activity via AKT phosphorylation. Thus, our study shows that the bidirectional crosstalk between TrTSC and TME results in a pro-tumorigenic and immunosuppressive contexture.

2021-07-02 | GSE136256 | GEO

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