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Cancer-associated fibroblasts metabolic targeting overcomes T-cell exclusion and chemoresistance [Mouse]

ABSTRACT: Cancer-associated fibroblasts metabolic targeting overcomes T-cell exclusion and chemoresistance [Mouse]

PROVIDER: PRJNA996082 | ENA |

REPOSITORIES: ENA

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Cancer-associated fibroblasts metabolic targeting overcomes T-cell exclusion and chemoresistance

Project description:Cancer-associated fibroblasts metabolic targeting overcomes T-cell exclusion and chemoresistance

| PRJNA996074 | ENA

Cancer-associated fibroblasts metabolic targeting overcomes T-cell exclusion and chemoresistance [Human]

Project description:Cancer-associated fibroblasts metabolic targeting overcomes T-cell exclusion and chemoresistance [Human]

| PRJNA996065 | ENA

Cancer-associated fibroblasts metabolic targeting overcomes T-cell exclusion and chemoresistance [Mouse]

Project description:T cell-based immunotherapies have exhibited promising outcomes in tumor control; however, their efficacy is limited in immune-excluded tumors. Cancer-associated fibroblasts (CAFs) play a pivotal role in shaping the tumor microenvironment and modulating T cell infiltration. Despite the identification of distinct CAF subtypes using single-cell RNA-sequencing, their specific impact on hindering T cell infiltration remains unclear, particularly in soft-tissue sarcomas (STS) characterized by low response rates to T cell-based therapies. In this study, we comprehensively characterized the STS microenvironment using murine models with distinct immune composition and scRNA-seq, leading to the identification of a unique subset of CAFs termed glycolytic cancer-associated fibroblasts (glyCAFs). GlyCAFs rely on glycolysis to impede cytotoxic T cell infiltration into the tumor parenchyma. Targeting glycolysis in glyCAFs enhances T-cell infiltration and augments the efficacy of chemotherapy. These findings highlight new avenues for combinatorial therapeutic interventions in sarcomas and other solid tumors. Further investigations and clinical trials are needed to validate these potential strategies and translate them into clinical practice.

2024-02-10 | GSE237636 | GEO

Cancer-associated fibroblasts metabolic targeting overcomes T-cell exclusion and chemoresistance [Human]

2024-02-10 | GSE237628 | GEO

Cancer-associated fibroblasts metabolic targeting overcomes T-cell exclusion and chemoresistance

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-02-06 | GSE237638 | GEO

Metabolic targeting of cancer associated fibroblasts overcomes T-cell exclusion and chemoresistance in soft-tissue sarcomas.

Project description:T cell-based immunotherapies have exhibited promising outcomes in tumor control; however, their efficacy is limited in immune-excluded tumors. Cancer-associated fibroblasts (CAFs) play a pivotal role in shaping the tumor microenvironment and modulating immune infiltration. Despite the identification of distinct CAF subtypes using single-cell RNA-sequencing (scRNA-seq), their functional impact on hindering T-cell infiltration remains unclear, particularly in soft-tissue sarcomas (STS) characterized by low response rates to T cell-based therapies. In this study, we characterize the STS microenvironment using murine models (in female mice) with distinct immune composition by scRNA-seq, and identify a subset of CAFs we termed glycolytic cancer-associated fibroblasts (glyCAF). GlyCAF rely on GLUT1-dependent expression of CXCL16 to impede cytotoxic T-cell infiltration into the tumor parenchyma. Targeting glycolysis decreases T-cell restrictive glyCAF accumulation at the tumor margin, thereby enhancing T-cell infiltration and augmenting the efficacy of chemotherapy. These findings highlight avenues for combinatorial therapeutic interventions in sarcomas and possibly other solid tumors. Further investigations and clinical trials are needed to validate these potential strategies and translate them into clinical practice.

| S-EPMC10954767 | biostudies-literature

Targeting PDGF signaling of cancer-associated fibroblasts blocks feedback activation of HIF-1α and overcomes chemoresistance in ovarian clear cell carcinoma

Project description:Targeting PDGF signaling of cancer-associated fibroblasts blocks feedback activation of HIF-1α and overcomes chemoresistance in ovarian clear cell carcinoma

| PRJNA930662 | ENA

Targeting DNA2 Overcomes Metabolic Reprogramming in Multiple Myeloma

Project description:Targeting DNA2 Overcomes Metabolic Reprogramming in Multiple Myeloma

| PRJNA807285 | ENA

Targeting IRAK1-S100A9 Axis Overcomes the Resistance to Paclitaxel in Nasopharyngeal Carcinoma

Project description:Resistance to chemotherapy is one of the main causes of mortality in late-stage nasopharyngeal carcinoma (NPC) with dismal prognosis and limited therapeutic options. Therefore, there is an urgent need to exploit new therapeutic targets to improve current clinical outcome. In this study, we identified pacritinib, a late stage clinical drug targeting IRAK1, as a sensitizer to resistance of paclitaxel in NPC. Through analysis of both chemoresistant cellular models and clinical samples of relapse and metastasis, we have shown that aberrant IRAK1-S100A9 deregulation is correlated with chemoresistance and prognosticates poor clinical outcome. Further functional studies demonstrated that genetic and pharmacological inhibition of IRAK1-S100A9 axis overcomes the resistance to paclitaxel and combination of pacritinib with paclitaxel exhibited superior anti-tumor effect in both in vivo and in vitro models.

2023-06-24 | GSE153125 | GEO

Targeting heparanase overcomes chemoresistance and diminishes relapse in myeloma.

Project description:In most myeloma patients, even after several rounds of intensive therapy, drug resistant tumor cells survive and proliferate aggressively leading to relapse. In the present study, gene expression profiling of tumor cells isolated from myeloma patients after sequential rounds of chemotherapy, revealed for the first time that heparanase, a potent promoter of myeloma growth and progression, was elevated in myeloma cells that survived therapy. Based on this clinical data, we hypothesized that heparanase was involved in myeloma resistance to drug therapy. In several survival and viability assays, elevated heparanase expression promoted resistance of myeloma tumor cells to chemotherapy. Mechanistically, this enhanced survival was due to heparanase-mediated ERK signaling. Importantly, use of the heparanase inhibitor Roneparstat in combination with chemotherapy clearly diminished the growth of disseminated myeloma tumors in vivo. Moreover, use of Roneparstat either during or after chemotherapy diminished regrowth of myeloma tumors in vivo following therapy. These results provide compelling evidence that heparanase is a promising, novel target for overcoming myeloma resistance to therapy and that targeting heparanase has the potential to prevent relapse in myeloma and possibly other cancers.

| S-EPMC4811483 | biostudies-literature

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