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

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

PROVIDER: PRJNA925019 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23106962_1.fastq.gz	Fastqsanger.gz
	SRR23106962_2.fastq.gz	Fastqsanger.gz
	SRR23106963_1.fastq.gz	Fastqsanger.gz
	SRR23106963_2.fastq.gz	Fastqsanger.gz
	SRR23106964_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 [HCT116]

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 | GSE223118 | GEO

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

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

| PRJNA925020 | ENA

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

2023-01-21 | GSE223119 | GEO

Gene expression profile of HCT116 exposed to chronic hypoxia

Project description:To identify genes involved in survival to prolonged hypoxia we exposed HCT116 to hypoxia for 3 days. Control cells were exposed to normoxic conditions. HCT116 colon cancer cells were serum starved and exposed to hypoxia (1%O2) or normoxia (21%O2) for 3 days.

2013-01-18 | E-GEOD-43608 | biostudies-arrayexpress

Integrated Omics Profiling Identifies Hypoxia-Regulated Genes in HCT116 Colon Cancer Cells

Project description:Hypoxia is associated with poor prognosis in most solid tumors due to its multiple effects on therapy resistance, angiogenesis, apoptotic resistance, and tumor invasion/metastasis. Here we used a comprehensive omics profiling to investigate hypoxia-regulated gene expression in HCT116 colon cancer cells. Quantitative analyses of proteome and secretome were performed in HCT116 cells cultured under hypoxic or normoxic conditions. A total of 5,700 proteins were quantified in proteome analysis and 722 proteins were quantified in secretome analysis. Both datasets were combined with the transcriptome and translatome datasets for further analysis. Verification of candidate proteins/genes in this integrated omics analysis was performed using immunoblotting and quantitative real-time RT-PCR analyses. We also performed polysome profiling to assess changes in translational efficiency of hypoxia-induced genes. Notably, several genes were differently regulated at the transcriptional and translational levels in HCT116 cells during hypoxia. Bioinformatics analysis suggested that hypoxia regulates translation of genes involved in extracellular matrix organization, extracellular exosomes, and protein processing in endoplasmic reticulum. Aberrations in these metabolic pathways appear to be correlated with an increased risk of tumor invasion/metastasis.

2018-03-14 | PXD009009 | Pride

Gene expression profile of HCT116 exposed to chronic hypoxia

Project description:To identify genes involved in survival to prolonged hypoxia we exposed HCT116 to hypoxia for 3 days. Control cells were exposed to normoxic conditions.

2013-01-18 | GSE43608 | GEO

PRO-seq from HCT116 cells in normoxia and hypoxia

Project description:PRO-seq analysis was used to examine rapid transcriptional changes in response to short-term hypoxia in WT and HIF1A-/- HCT116 cells

2021-01-29 | GSE145567 | GEO

PolyA RNAseq from HCT116 cells in normoxia and hypoxia

Project description:To determine the effects of depleting TIP60, CDK8, or HIF1A on the transcriptional response to hypoxia, we performed RNAseq analysis of four HCT116 colorectal carcinoma cell lines (shNT, HIF1A-/-, shTIP60 and shCDK8) in normoxic and hypoxic (24hrs, 1% O2) conditions. PolyA RNA for two independent biological replicates was purified from HCT116 cells stably expressing an shRNA against a non-targeting control (shNT), TIP60 (shTIP60) or CDK8 (shCDK8), or genetically deleted HIF1A (HIF1A-/-) subjected to 24hrs 1% O2 (hypoxia) or maintained under ambient oxygen (21%; normoxia) was sequenced on the Ion Torrent platform. Reads were aligned to the human genome and gene-level counts were used for differential expression analysis.

2016-06-02 | E-GEOD-68297 | biostudies-arrayexpress

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

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