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

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

PROVIDER: PRJNA898814 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22207387_1.fastq.gz	Fastqsanger.gz
	SRR22207387_2.fastq.gz	Fastqsanger.gz
	SRR22207388_1.fastq.gz	Fastqsanger.gz
	SRR22207388_2.fastq.gz	Fastqsanger.gz
	SRR22207389_1.fastq.gz	Fastqsanger.gz

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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

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

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

Inhibition of cancer cell self-renewal through an epigenetic HDACi-histone H1.0 axis.

Project description:Identification of HDACi-responsive, H1.0-dependent genes inhibiting self-renewal of HCC1569 breast cancer cells.

2020-02-20 | GSE119369 | GEO

Genome Wide Distribution of Linker Histone H1.0 is Independent of MeCP2 I

Project description:Previous studies suggested that MeCP2 binds to linker DNA and competes with linker histone H1 to regulate chromatin structure, but this hypothesis has never been tested in vivo. Here, we expressed Flag-tagged H1.0 in forebrain excitatory neurons in mice and performed ChIP-Seq to reveal H1.0 distribution and its relationship with MeCP2. Unexpectedly, we detected no major change in H1.0 upon MeCP2 depletion, revealing that MeCP2 functions independent of linker H1.0.

2018-05-28 | GSE95471 | GEO

Genome Wide Distribution of Linker Histone H1.0 is Independent of MeCP2 II

2018-05-28 | GSE107519 | GEO

L-Glutamine metabolism and its regulation in C. glutamicum

Project description:Corynebacterium glutamicum, a gram-positive soil bacterium used for the industrial production of amino acids such as L-glutamate and L-lysine, is able to use a number of different nitrogen sources, such as ammonium, urea, or creatinine. In this communication, we show that L-glutamine serves as an excellent nitrogen source for C. glutamicum and allows similar growth rates in glucose minimal medium as ammonium. A transcriptome comparison revealed a strong induction of the nitrogen starvation response when glutamine was used as nitrogen source. Subsequent growth experiments with a variety of mutants defective in nitrogen metabolism showed that glutamate synthase is crucial for glutamine utilization, while a putative glutaminase is dispensable under the experimental conditions used. The fact that the glutamate synthase encoding gltBD operon is under strict nitrogen control explains the necessity for induction of the nitrogen starvation response. The paradox situation that the nitrogen starvation response is induced although intracellular L-glutamine levels are high has implications on nitrogen sensing. In contrast to other gram-positive and gram-negative bacteria such as Bacillus subtilis, Salmonella typhimurium, and Klebsiella pneumoniae, a drop in glutamine concentration obviously does not serve as a nitrogen starvation signal in C. glutamicum.

2010-10-05 | GSE19779 | GEO

L-Glutamine metabolism and its regulation in C. glutamicum

2010-10-05 | E-GEOD-19779 | biostudies-arrayexpress

Short-term Starvation vs. Normal Diet Before Chemotherapy of Solid Tumors

Project description:Recent pre-clinical data provide strong evidence that short-term starvation before the administration of cytostatic drugs for the chemotherapy of solid tumors leads to significantly higher efficacy and lower toxicity levels. However, these findings have so far not been validated in patients. The aim of this trial is to provide first clinical evidence regarding the impact of pre-chemotherapeutic short-term starvation on response to therapy (primary endpoint). Additionally, progression-free survival, adverse events, and overall survival will be monitored (secondary endpoints). In perspective, short-term starvation before chemotherapy could represent a simple and secure way to improve both efficacy and tolerance of chemotherapies at low cost.

| 2202552 | ecrin-mdr-crc

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

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

| PRJNA561847 | ENA