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ATAC-seq analysis in KPC1199 murine PDAC cell line with or without glutamine starvation

ABSTRACT: ATAC-seq analysis in KPC1199 murine PDAC cell line with or without glutamine starvation

PROVIDER: PRJNA952642 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24087580_1.fastq.gz	Fastqsanger.gz
	SRR24087580_2.fastq.gz	Fastqsanger.gz
	SRR24087581_1.fastq.gz	Fastqsanger.gz
	SRR24087581_2.fastq.gz	Fastqsanger.gz
	SRR24087582_1.fastq.gz	Fastqsanger.gz

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ATAC-seq analysis in KPC1199 murine PDAC cell line with or without glutamine starvation

Project description:We determined if up- and/or down-regulated genes in pancreatic tumor cells cultured under low-glutamine conditions were accompanied by alterations in genome-wide chromatin accessibility and then performed ATAC-seq of KPC1199 cells treated with low glutamine concentrations versus normal-media-treated controls. The ATAC-seq was performed according to the TruePrep Tagment Enzyme for ATACseq kit (TD501, Vazyme). DNA libraries were constructed following the manufacturer’s instructions of the Trueprep index kit v2 (TD202, Vazyme) and thereafter sequenced to an average of 20 million reads per sample.

2024-04-30 | GSE229051 | GEO

CUT&Tag analysis of H3K4me3, H3K27Ac,H2A119Ub, H3K27me3 and H3K36me3 in KPC1199 murine PDAC cell line

Project description:To gain mechanistic insight into how Epigenetic factors reprogramming metabolism in response to glutamine starvation. we performed CUT&Tag sequencing in murine PDAC cells. KPC1199 cells were treated in Cont group or Low Gln group , and harvested after 72 hours. CUT&Tag assay was performed following the manual of hyperactive pG-Tn5/pA-Tn5 transposase for CUT&Tag kit (TD901, Vazyme). DNA library were prepared according to manufacturer’s instructions of Trueprep index kit v2 (TD202, Vazyme).

2024-12-31 | GSE229903 | GEO

The role of compensatory metabolic reprogramming in ensuring PDAC cell survival under the limitation of glutamine

Project description:KPC1199 cells were treated in Cont group(2 mmol/L glutamine and 2.25 g/L glucose) or Low Gln group (0.4 mmol/L glutamine and 2.25 g/L glucose) , and harvested after 72 hours for RNA preparation.

2024-12-31 | GSE229055 | GEO

Phosphoethanolamine Accumulation Protects Cancer Cells under Glutamine Starvation through Downregulation of PCYT2

Project description:The conditions of the tumor microenvironment, such as nutrient starvation, play critical roles in cancer progression. However, the role of glutamine deprivation in cancer progression is not studied as extensively as that of hypoxia. Here, we show that glutamine starvation triggered down-regulation of PCYT2 by stimulating accumulation of PEtn. Interestingly, glutamine upregulated series of glutamine-responsive genes, not only PCYT2. Furthermore, glutamine-responsive genes were associated with overall survival of cancer patients. Thus, our findings show that glutamine responsive genes such as PCYT2 are key for progression of cancer cells, partly protecting cancer cells to glutamine starvation.

2019-08-24 | GSE136289 | GEO

CUT&Tag analysis of H3K4me3, H3K27Ac,H2A119Ub and H3K27me3 in treated KPC1199 murine PDAC cell line

Project description:To gain mechanistic insight into how Epigenetic factors reprogramming tumor immune microenvironment in response to IFNγ stimulation. we performed CUT&Tag sequencing in murine PDAC cells.For comparison of the transcription profile between IFNγ-PD-L1all and IFNγ+PD-L1all cells, we treated KPC1199 cells with vehicle control or 10 ng/mL recombinant mouse IFNγ for 20 hours and harvested them. For comparison of PD-L1hi with PD-L1all, cells were either sorted with the top 15% PD-L1+ or total of IFNγ+PD-L1all PDAC cells, and freshly collected as soon as possible. Hyperactive pA-Tn5 Transposase for CUT&Tag kit from Vazyme (TD901), and antibodies against H3K4me3 from Abcam (ab213224), H3K27Ac from Abcam (ab4729),H2A119Ub from Cell Signaling (8240T) and H3K27me3 from Abcam (ab6002) were employed. Trueprep index kit v2 and v3 for illumina were used to establish DNA library.

2024-08-20 | GSE222133 | GEO

A role for p53 in the adaptation to glutamine starvation through the expression of Slc1a3

Project description:Numerous mechanisms to support cells under conditions of transient nutrient starvation have been described. The tumor suppressor protein p53 can contribute to the adaptation of cells to metabolic stress through various mechanisms that may help cancer cell survival in nutrient limiting conditions. We show here that p53 helps cancer cells to survive glutamine starvation by promoting the expression of SLC1A3, an aspartate/glutamate transporter that allows the utilization of aspartate to support cells in the absence of extracellular glutamine. Under glutamine deprivation, SLC1A3 expression maintains electron transport chain and tricarboxylic acid cycle activity, promoting de novo glutamate, glutamine and nucleotide synthesis to rescue cell viability. Tumor cells with high levels of SLC1A3 expression are resistant to glutamine starvation and SLC1A3 depletion retards the growth of these cells in vitro and in vivo, suggesting a therapeutic potential for SLC1A3 inhibition.

2018-06-28 | GSE116087 | GEO

IFRD1 promotes tumor cells “low-cost” survival under glutamine starvation via inhibiting histone H1.0 nucleophagy

Project description:Glutamine addiction represents a metabolic vulnerability of cancer cells although effective therapeutic targeting of the pathways involved remains to be realized. Here, we disclose the critical role of IFRD1 (interferon-related developmental regulator 1) in the adaptive survival of hepatocellular carcinoma cells (HCC) during glutamine starvation. The induction and translocation of IFRD1 to the endoplasmic reticulum inhibits autophagy by promoting proteasomal degradation of the key autophagy regulator ATG14 in a TRIM21-dependent manner. On the contrary, enforced IFRD1 loss increases autophagy flux leading to cell death. This effect is largely realized through the autophagy-dependent degradation of histone H1.0 causing globally enhanced chromatin accessibility associated with unchecked increases in ribosome and protein biosynthesis . This in turn leads to metabolic exhaustion and death under glutamine starvation. Practically, IFRD1 depletion in preclinical HCC models potentiates glutamine limiting strategies including synergizing with the glutaminase-1 selective inhibitor CB-839. Thus, IFRD1 supports the adaptive survival of cancer cells under glutamine starvation, with potential as a therapeutic target in anti-cancer applications.

2024-03-23 | GSE217406 | GEO

CUT&Tag analysis of H3K4me3, H3K27Ac,H2A119Ub, H3K27me3 and H3K36me3 in KPC1199 murine PDAC cell line

Project description:CUT&Tag analysis of H3K4me3, H3K27Ac,H2A119Ub, H3K27me3 and H3K36me3 in KPC1199 murine PDAC cell line

| PRJNA956558 | ENA

CUT&Tag analysis of H3K4me3, H3K27Ac,H2A119Ub and H3K27me3 in treated KPC1199 murine PDAC cell line

Project description:CUT&Tag analysis of H3K4me3, H3K27Ac,H2A119Ub and H3K27me3 in treated KPC1199 murine PDAC cell line

| PRJNA918356 | ENA

Glutamine depletion regulates Slug to promote EMT and metastasis in pancreatic cancer [mouse]

Project description:Tumor cells rely on glutamine to fulfill their metabolic demands and sustain proliferation. The elevated consumption of glutamine can lead to intratumoral nutrient depletion, causing metabolic stress that has the potential to impact tumor progression. Here, we show that nutrient stress caused by glutamine deprivation leads to the induction of epithelial-mesenchymal transition (EMT) in pancreatic ductal adenocarcinoma (PDAC) cells. Mechanistically, we demonstrate that glutamine deficiency regulates EMT through the upregulation of the EMT master regulator Slug, a process that is dependent on both MEK/ERK signaling and ATF4. We find that Slug is required in PDAC cells for glutamine deprivation-induced EMT, cell motility and nutrient stress survival. Importantly, we decipher that Slug is associated with nutrient stress in PDAC tumors and is required for metastasis. These results delineate a novel role for Slug in the nutrient stress response and provide insight into how nutrient depletion might influence PDAC progression.

2020-05-20 | GSE150874 | GEO

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