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Cancer-associated fibroblast-specific lncRNA LINC01614 enhances glutamine uptake in lung adenocarcinoma

ABSTRACT: Cancer-associated fibroblast-specific lncRNA LINC01614 enhances glutamine uptake in lung adenocarcinoma

PROVIDER: PRJNA878825 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21504677_1.fastq.gz	Fastqsanger.gz
	SRR21504677_2.fastq.gz	Fastqsanger.gz
	SRR21504678_1.fastq.gz	Fastqsanger.gz
	SRR21504678_2.fastq.gz	Fastqsanger.gz
	SRR21504679_1.fastq.gz	Fastqsanger.gz

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Cancer-associated fibroblast-specific lncRNA LINC01614 enhances glutamine uptake in lung adenocarcinoma

Project description:To investigate the mechanism of CAF-exosome-packaged LINC01614 in the regulation of the glutamine metabolism of cancer cells.

2022-09-16 | GSE213043 | GEO

Glutamine deprivation enhances directed differentiation of renal organoids

Project description:Glutamine deprivation enhances directed differentiation of renal organoids

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Survival and Proliferation of T-cell Acute Lymphoblastic Leukaemia Depends on mTOR-regulated Glutamine Uptake and EAAT1 Activity

Project description:With the aim to identify new therapeutic targets for T-ALL treatment, we integrated transcriptomics and metabolomics data, including live-cell NMR-spectroscopy, of cell lines and patient samples. We found that T-ALL cells have limited energy availability, resulting in down-regulated mTOR-signalling and reduced autophagy. Despite this, mTOR kinase activity is essential for the glutamine-uptake and rapid proliferation. T-ALL cells use glutamine as a source for all nitrogen atoms in purines and for all but one carbon in pyrimidines. We show that EAAT1, the glutamate-aspartate transporter normally only expressed in the CNS, is a crucial facilitator of the glutamine conversion to nucleotides. T-ALL cell proliferation depends on EAAT1 function, identifying it as a target for T-ALL treatment.

2020-11-01 | GSE101566 | GEO

Macropinocytosis mediates resistance to loss of glutamine transport in triple-negative breast cancer

Project description:Triple-negative breast cancer (TNBC) relies on glutamine uptake by the transporter ASCT2 to sustain their unique glutamine metabolism and growth. Despite previous data showing cell growth inhibition after ASCT2 knockdown, ASCT2 CRISPR knockout was well-tolerated by breast cancer cell lines. Despite the loss of a glutamine transporter and low rate of glutamine uptake, intracellular glutamine steady state levels were higher in ASCT2 knockout compared to control TNBC cells. Proteomics data revealed upregulation of macropinocytosis, reduction in glutamine efflux and glutamine synthesis in ASCT2 knockout cells. Loss of ASCT2 in TNBC cell line HCC1806 induced a 5-10-fold increase in macropinocytosis across 5 separate ASCT2 knockout clones, compared to a modest 2-fold increase in the shRNA ASCT2 knockdown. By comparison, ASCT2 knockout impaired cell proliferation in a non-macropinocytic breast cancer cell line, HCC1569. These data suggest that macropinocytosis provides a novel resistance mechanism to strategies targeting glutamine uptake alone. Despite this adaptation, TNBC cells continue to rely on glutamine metabolism for their growth, which suggests therapeutic targeting may need to focus on downstream glutamine metabolism pathways.

2024-09-15 | GSE256218 | GEO

p53 promotes cancer cell adaptation to glutamine deprivation by upregulating Slc7a3 to increase arginine uptake

Project description:Cancer cells heavily depend on the amino acid, glutamine, to meet the demands associated with growth and proliferation. Due to its rapid consumption, cancer cells frequently undergo glutamine starvation in vivo. We and others have shown that p53 is a critical regulator in metabolic stress resistance. To better understand the molecular mechanisms by which p53 activation promotes cancer cell adaptation to glutamine deprivation, we identified p53-dependent genes that are induced upon glutamine deprivation using RNA-seq analysis. We show that Slc7a3, an arginine transporter, is significantly induced by p53. We show the concomitant rise in intracellular arginine levels following glutamine deprivation is dependent on p53. The influx of arginine has minimal effect on known metabolic pathways upon glutamine deprivation. Instead, we found arginine serves as an effector for mTORC1 activation to promote in vitro and in vivo cell growth in response to glutamine starvation. Therefore, we identify a novel p53-inducible gene that contributes to the metabolic stress response.

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Bone Stromal Glutamine Renders Tumor cell PARP Inhibitor Resistance

Project description:The majority of patients with late-stage breast cancer develop distal bone metastases. The bone microenvironment can affect response to therapy, and uncovering the underlying mechanisms could help identify improved strategies for treating bone metastatic breast cancer. Here, we observed that osteoclasts reduced the sensitivity of breast cancer cells to DNA damaging agents, including cisplatin and the PARP inhibitor (PARPi) olaparib. Metabolic profiling identified elevated glutamine production by osteoclasts. Glutamine supplementation enhanced the survival of breast cancer cells treated with DNA damaging agents, while blocking glutamine uptake increased sensitivity and suppressed bone metastasis. GPX4, the critical enzyme responsible for glutathione oxidation, was upregulated in cancer cells following PARPi treatment through stress-induced ATF4-dependent transcriptional programming. Increased glutamine uptake and GPX4 upregulation concertedly enhanced glutathione metabolism in cancer cells to help neutralize oxidative stress and generate PARPi resistance. Analysis of paired patient samples of primary breast tumors and bone metastases revealed significant induction of GPX4 in bone metastases. Combination therapy utilizing PARPi and zoledronate, which blocks osteoclast activity and thereby reduces the microenvironmental glutamine supply, generated a synergistic effect in reducing bone metastasis. These results identify a role for glutamine production by bone-resident cells in supporting metastatic cancer cells to overcome oxidative stress and develop resistance to DNA-damaging therapies.

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ASCT2 is a major contributor to serine uptake in cancer cells

Project description:The non-essential amino acid serine is a critical nutrient for cancer cells due to its diverse biosynthetic functions. While some tumors can synthesize serine de novo, others are auxotrophic and therefore reliant on serine uptake. Importantly, despite several transporters being known to be capable of transporting serine, the transporter(s) that mediate serine uptake in cancer cells are not known. Here, we characterize the amino acid transporter ASCT2 (SLC1A5) as a major contributor to serine uptake in cancer cells. ASCT2 is well-known as a glutamine transporter in cancer, and our work demonstrates that serine and glutamine compete for uptake through ASCT2. We further show that ASCT2-mediated serine uptake is essential for purine nucleotide biosynthesis and that ERα promotes serine uptake by directly activating SLC1A5 transcription. Together, our work defines an additional important role for ASCT2 as a serine transporter in cancer and evaluates ASCT2 as a potential therapeutic target.

2024-06-11 | GSE269606 | GEO

Expression data from TH17 cells cultured in the presence or absence of glutamine

Project description:T cell fate and function is closely related to nutrient uptake and utilization. Here we demonstrate that glutamine deprivation switch Th17 cells to Treg cells in a time and dose dependent manner. The finding highlight the critical role of glutamine in T cell fate determination through a metabolic-epigenetic axis. We performed microarrays to explore the gene expression pattern of TH17 cells in the presence or absence of glutamine.

2024-02-09 | GSE166430 | GEO

p53 promotes cancer cell adaptation to glutamine deprivation by upregulating Slc7a3 to increase arginine uptake

Project description:p53 promotes cancer cell adaptation to glutamine deprivation by upregulating Slc7a3 to increase arginine uptake

| PRJNA517491 | ENA

Effect of glutamine supplementation on naïve CD4 T cell differentiation from CARD11 R75W mutation patients

Project description:CARD11 LOF mutant patients develop severe atopic phenotpes and increased T-helper 2 (Th2) cytokine production, in addition to other immunopathology. CARD11 LOF impairs lymphocyte receptor–mediated glutamine uptake—thereby reducing signaling in mTORC1. Herein, we investigate whether exogenous glutamine treatment would alleviate Th2 phenotypes of CARD11 LOF mutant T cells.

2025-01-20 | GSE287077 | GEO

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