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GLUT3/SLC2A3 is an endogenous marker of hypoxia in prostate epithelial and prostate cancer cells.

ABSTRACT: GLUT3/SLC2A3 is an endogenous marker of hypoxia in prostate epithelial and prostate cancer cells.

PROVIDER: PRJNA806639 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18004600.fastq.gz	Fastqsanger.gz
	SRR18004601.fastq.gz	Fastqsanger.gz
	SRR18004590.fastq.gz	Fastqsanger.gz
	SRR18004591.fastq.gz	Fastqsanger.gz
	SRR18004592.fastq.gz	Fastqsanger.gz

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GLUT3/SLC2A3 is an endogenous marker of hypoxia in prostate epithelial and prostate cancer cells.

Project description:The microenvironment of solid tumors is dynamic and frequently contain pockets of low oxygen levels (hypoxia) surrounded by regions of normal oxygen levels. Indeed, a compromised vascular is a is hallmark of the tumor microenvironment, creating gradients of hypoxia. Notably, hypoxia associates with increased metastasis and poor survival in patients. Therefore, to aid therapeutic decisions and better understand hypoxia's role in cancer progression, it is critical to identify endogenous biomarkers of hypoxia to spatially phenotype oncogenic lesions in human tissue, whether precancerous, benign, or malignant. Here, we characterize the glucose transporter GLUT3/SLC2A3 as a biomarker of hypoxia prostate epithelial cells and prostate tumors. Transcriptomic analyses of hypoxic immortalized prostate epithelial cells revealed a highly significant increase in GLUT3 expression. GLUT3 upregulation was also detected by immunostaining in hypoxic prostate epithelial cells and prostate cancer cell lines. Additionally, GLUT3 dramatically co-localized with the hypoxia-marker pimonidazole in xenograft tumors formed from prostate cancer cells and showed distinct concentration gradients within patient-derived xenograft tumors from primary and metastatic prostate cancer. Compared to established hypoxia-response genes, GLUT1 and CA9, GLUT3 shows a higher degree of hypoxia labeling within tumor tissue and may serve as a alternative endogenous biomarker of hypoxia.

2022-02-16 | GSE196634 | GEO

Transcriptomic profiling of multiple tissues from aged mice with endothelial-specific Slc2a3 (GLUT3) overexpression

Project description:Aging is accompanied by progressive alterations in vascular endothelial function and tissue homeostasis. Glucose transporter 3 (GLUT3), encoded by Slc2a3, is a high-affinity glucose transporter that may influence endothelial metabolism and systemic tissue homeostasis. To investigate whether endothelial-specific GLUT3 overexpression modulates age-associated transcriptional changes across multiple organs, we performed RNA sequencing of tissues collected from 24-month-old wild-type (WT) mice and mice with endothelial-specific Slc2a3 overexpression (R26-LSL-Slc2a3;Cdh5-2A-CreERT2, KI). Ten tissues, including heart, liver, spleen, lung, kidney, small intestine, brown adipose tissue (BAT), hindlimb skeletal muscle, skin, and brain, were collected from three biological replicates per group. This dataset provides a comprehensive multi-tissue transcriptomic resource for evaluating the effects of endothelial GLUT3 overexpression on age-associated molecular alterations and inter-organ responses in aged mice.

2026-08-22 | GSE343755 | GEO

GLUT3 salvage with vitamin C treatment altered gene expression landscape of OCI-AML3

Project description:To investigate the GLUT3 salvage-induced transcriptome changes, we performed RNA-seq on the SLC2A3 overexpressed and the empty control OCI-AML3 cell lines treated with 250 µM of vitamin C.

2023-04-25 | GSE216576 | GEO

GLUT3/SLC2A3 Is an Endogenous Marker of Hypoxia in Prostate Cancer Cell Lines and Patient-Derived Xenograft Tumors.

Project description: Not available

| S-EPMC8946944 | biostudies-literature

A Distinct Role for GLUT3 in Glioblastoma Invasion

Project description:In a study of GLUT1 and GLUT3, we used RNA-sequencing to assess the affects of GLUT1 and GLUT3 knockdown in the D456 glioblastoma cell line.

2020-07-01 | GSE148739 | GEO

Transcriptomic profiling of multiple tissues from aged mice with endothelial-specific Slc2a3 (GLUT3) overexpression

Project description:Transcriptomic profiling of multiple tissues from aged mice with endothelial-specific Slc2a3 (GLUT3) overexpression

| PRJNA1512502 | ENA

GBM-derived Exosomes Containing GLUT3 Increase the Migratory Potential of Monocytes

Project description:Glioblastoma (GBM) remains a challenging malignancy with dismal prognoses despite aggressive treatment regimens. Intratumoral heterogeneity contributes to therapeutic resistance, with roles for stem cell-like brain tumor initiating cells (GBMs), glioma associated macrophages (GAMs), and communication between them. GAMs are derived from infiltrating lymphocytes, and monocyte migration is increased by GBM cell release of extracellular vesicles, including exosomes. GBM survival is promoted by the glucose transporter GLUT3, which was recently shown to alter macrophage activation states. We found that GBM-derived exosomes contain GLUT3 and that exosomes from GLUT3 expressing GBMs significantly increased monocyte migration in comparison to controls. Monocytes transfected with GLUT3 (but not GLUT1) also had significantly increased migration, demonstrating a direct role for GLUT3 in monocytes migration. Analysis of the transcriptome of exosome treated monocytes demonstrated that exosomes derived from GLUT3 expressing GBMs increasedGDF-15in monocytes. GDF-15 is a known regulator of monocyte migration, and we determined that knockdown of GDF-15 blocked the migration induced by GBM-derived exosomes. As GDF-15 induced monocyte migration is thought to involve MMP12, we next evaluated MMP12 as a potential mediator of the pro-migratory phenotype.MMP12was significantly increased in monocytes upon treatment with exosomes derived from GLUT3 expressing GBMs as was MMP12 activity. Together, our findings suggest a novel mechanism by which GBMs facilitate immune evasion and tumor progression: GBM-derived exosomes transfer GLUT3 to monocytes to increase a GDF-15/MMP12 pathway that promotes monocyte migration. The data also highlight the importance of understanding and targeting cell-cell interactions to improve glioblastoma treatment.

2024-12-01 | GSE274966 | GEO

Effects of GLUT3 on transcription and translation in aged primary HUVECs

Project description:Young HUVECs were infected with lentivirus to overexpress GLUT3, and a replicative senescence cell model was established through replicative passaging. Subsequently, mRNA-seq and Ribo-seq were performed on young HUVECs, replicatively senescent HUVECs, and GLUT3-overexpressing replicatively senescent HUVECs.

2026-07-04 | GSE336332 | GEO

RNA-seq of wild type and GLUT3-deficient T helper 17 (Th17) cells

Project description:RNA-sequencing and analysis of in vitro differentiated Th1 and Th17 cells isolated from WT and Slc2a3-fl/fl Cd4-cre mice.

2022-02-13 | GSE192659 | GEO

On-demand GLUT3 expression augments CAR-T cell metabolic fitness and antitumor efficacy whereas preventing toxicity in glioblastoma

Project description:We show that the dysfunction of CAR-T cells in GBM is attributed to glucose deficiency in the tumor microenvironment (TME) and that on-demand, but not continuous, metabolic replenishment significantly improves the antitumor efficacy of CAR-T cells. The massive consumption of glucose by cancer cells reduces the glucose level in the TME of GBM, consequently impairing CAR-T cells. Adding stable expression of glucose transporter 3 (GLUT3), a high-affinity glucose transporter, to CAR-T cells restored their cytokine production and killing activity. However, whereas CAR-T cells with stable GLUT3 expression induced tumor reduction in a GBM model, their overactivation led to adverse events and mouse death. On-demand GLUT3-expressing CAR-T cells, in which GLUT3 transcription is driven by the nuclear translocation of nuclear factor of activated T cells (NFAT) by target antigen stimulation, exhibited enhanced metabolic fitness and increased antitumor efficacy, leading to long-lasting tumor control in intracranial human GBM cell xenograft models whereas it prevented adverse events.

2026-04-16 | GSE320375 | GEO

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