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Hypoxia-induced cysteine metabolism reprogramming are crucial for the tumorigenesis of colorectal cancer [tissue pair]

ABSTRACT: Hypoxia-induced cysteine metabolism reprogramming are crucial for the tumorigenesis of colorectal cancer [tissue pair]

PROVIDER: PRJNA925020 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23107000_1.fastq.gz	Fastqsanger.gz
	SRR23107000_2.fastq.gz	Fastqsanger.gz
	SRR23107001_1.fastq.gz	Fastqsanger.gz
	SRR23107001_2.fastq.gz	Fastqsanger.gz
	SRR23107002_1.fastq.gz	Fastqsanger.gz

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Hypoxia-induced cysteine metabolism reprogramming are crucial for the tumorigenesis of colorectal cancer.

Project description:Hypoxia-induced cysteine metabolism reprogramming are crucial for the tumorigenesis of colorectal cancer.

| PRJNA925018 | ENA

Hypoxia-induced cysteine metabolism reprogramming are crucial for the tumorigenesis of colorectal cancer [tissue pair]

Project description:Metabolic reprogramming is a hallmark of human cancer and cancer-specific metabolism provide opportunities for cancer diagnosis, prognosis, and treatment. However, how metabolic pathways affect the initiation and progression of colorectal cancer remain largely unknown. Here, we showed cysteine is highly enriched in colorectal tumors compared with adjacent non-tumor tissues to promote tumorigenesis of CRC. Both cystine and cysteine imports are essential to maintain intracellular cysteine level and promote tumor growth and survival. Transporter genes of cystine and cysteine are all upregulated in colorectal cancer by tumor microenvironment induced ROS through transcription factor ATF4. Glutathione synthetase GSS is upregulated and increases cysteine to reduced glutathione flux to support tumor growth and survival in colorectal cancer. Depletion of cystine and cysteine by a recombinant cyst(e)inase effectively reduced the growth of colorectal tumors. Moreover, scavenging cystine and cysteine induces autophagy of colorectal cancer cells through mTOR-ULK signaling axis. With this study, we demonstrate that cysteine metabolism is a key signature of CRC metabolic reprogramming and targeting cysteine metabolism might be an effective approach to treat colon cancer.

2023-01-21 | GSE223119 | GEO

Hypoxia-induced cysteine metabolism reprogramming are crucial for the tumorigenesis of colorectal cancer [HCT116]

Project description:Hypoxia-induced cysteine metabolism reprogramming are crucial for the tumorigenesis of colorectal cancer [HCT116]

| PRJNA925019 | ENA

Hypoxia-induced cysteine metabolism reprogramming are crucial for the tumorigenesis of colorectal cancer [HCT116]

2023-01-21 | GSE223118 | GEO

Hypoxia-induced cysteine metabolism reprogramming is crucial for the tumorigenesis of colorectal cancer.

Project description:Metabolic reprogramming is a hallmark of human cancer, and cancer-specific metabolism provides opportunities for cancer diagnosis, prognosis, and treatment. However, the underlying mechanisms by which metabolic pathways affect the initiation and progression of colorectal cancer (CRC) remain largely unknown. Here, we demonstrate that cysteine is highly enriched in colorectal tumors compared to adjacent non-tumor tissues, thereby promoting tumorigenesis of CRC. Synchronously importing both cysteine and cystine in colorectal cancer cells is necessary to maintain intracellular cysteine levels. Hypoxia-induced reactive oxygen species (ROS) and ER stress regulate the co-upregulation of genes encoding cystine transporters (SLC7A11, SLC3A2) and genes encoding cysteine transporters (SLC1A4, SLC1A5) through the transcription factor ATF4. Furthermore, the metabolic flux from cysteine to reduced glutathione (GSH), which is critical to support CRC growth, is increased due to overexpression of glutathione synthetase GSS in CRC. Depletion of cystine/cysteine by recombinant cyst(e)inase effectively inhibits the growth of colorectal tumors by inducing autophagy in colorectal cancer cells through mTOR-ULK signaling axis. This study demonstrates the underlying mechanisms of cysteine metabolism in tumorigenesis of CRC, and evaluates the potential of cysteine metabolism as a biomarker or a therapeutic target for CRC.

| S-EPMC11340627 | biostudies-literature

Hypoxia-induced cysteine metabolism reprogramming are crucial for the tumorigenesis of colorectal cancer.

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

2023-01-21 | GSE223120 | GEO

Effect of PCO1 overexpression [hypoxia]

Project description:The effect of the overexpression of Plant Cysteine Oxidase (PDCO1) on the transcriptome of Arabidopsis resettes was investigated with plants subjected to a 4h hypoxia (5% O2 v/v in air). For this purpose, 4-week old rosette of wild-type and 35S:FLAG:CDO1 plants were compared. Samples were composed of pools of 5 plants. In total, 6 samples were analyzes, subdivided in 2 thesis with 3 replicates each. 35S:PCO1 plants (treated with hypoxia) were compared to wild-type plants (treated with hypoxia).

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Identification of hypoxia-inducible genes in Arabidopsis mesophyll cells

Project description:The goal of this experiment was to investigate the early transcript changes (6h) induced by hypoxia treatment in mesophyll protoplasts. A single pair (control & hypoxia) of GeneChips® was used to confirm that hypoxia treatment altered the expression of an overlapping set of genes controlled by KIN10 (At3g01090) in Arabidopsis mesophyll protoplasts. Keywords: KIN10, KIN11, darkness, hypoxia, starvation, stress, sugar signalling, Arabidopsis, SnRK1

2007-08-17 | GSE8248 | GEO

Cysteine deprivation in liver cell line

Project description:First experiment: Cells were cultured in sulfur amino acid-free DMEM supplemented with 0.1 mM methionine + 0.1 mM cysteine (complete) or supplemented only with 0.1 mM methionine (cysteine-free). Cells were cultured in either medium for 42 h (Long + Cys; Long -Cys) or in cysteine-free medium for 36 h followed by 6 h in complete medium (Short +Cys) Second experiment: C3A/HepG2 cells were cultured in sulfur amino acid-free DMEM supplemented with 0.1 mM Met and 0.1 mM Cys (complete) or supplemented only with 0.1 mM Met (cysteine-devoid). Cells were cultured in complete medium for 42 h (Long +Cys) or in complete medium for 36 h followed by cysteine-devoid medium for 6 h (Short -Cys). Keywords: amino acid deprivation

2007-12-13 | GSE9517 | GEO

Pair bonding and disruption impact lung transcriptome in monogamous Peromyscus californicus

Project description:To investigate the effects of bonding experiences on the transcriptome of monogamous P. californicus in the lungs. Our results indicated that the lung transcriptomes of Peromyscus californicus are altered in a manner that depends on pair bonding. Pathways affected include hypoxia response and heart development.

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