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

ABSTRACT: Glutamine depletion regulates Slug to promote EMT and metastasis in pancreatic cancer [human]

PROVIDER: PRJNA633899 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11813358.fastq.gz	Fastqsanger.gz
	SRR11813359.fastq.gz	Fastqsanger.gz
	SRR11813360.fastq.gz	Fastqsanger.gz
	SRR11813361.fastq.gz	Fastqsanger.gz
	SRR11813362.fastq.gz	Fastqsanger.gz

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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

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

2020-05-20 | GSE150873 | GEO

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

Project description:Glutamine depletion regulates Slug to promote EMT and metastasis in pancreatic cancer

| PRJNA633897 | ENA

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

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

| PRJNA633900 | ENA

Glutamine depletion regulates Slug to promote EMT and metastasis in pancreatic cancer.

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 up-regulation 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.

| S-EPMC7478719 | biostudies-literature

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

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

2020-05-20 | GSE150875 | GEO

SLUG is enhanced by chemotherapeutics and functions to promote invasion and metastasis by directly targeting MMP3 in Cervical Cancer

Project description:Neoadjuvant chemotherapy (NACT) followed by radical surgery for patients in FIGO stages IB2-IIB has proven to reduce tumor volume and numbers. However, NACT followed by radical surgery has not been found to improve overall survival. In this study, 35 paired pre/post-NACT cervical cancer tissues and 167 cervical cancer samples were examined by immunohistochemical analysis, SLUG expression was potentially increased in cervical cancer tissues after neoadjuvant chemotherapy, which in turn positively correlated with pelvic lymph node metastasis. The expression of SLUG following neoadjuvant chemotherapy was identified as a poor survival indicator. Functional assays, Agilent microarray hybridization and CHIP assay were performed to determine SLUG’s downstream genes and pathways. SLUG overexpression promoted metastasis in cervical cancer in both in vitro and in vivo models, whereas SLUG silencing had the opposite effect. Mechanically, SLUG is not a prerequisite for EMT activation in cervical cancer models, but contributes to the invasiveness and metastasis of cervical cancer cells by directly tethering to the recognition sequence GCCAGGTGC in the MMP3 promoter region. Our results provide mechanistic insight into the potential pro-cancer effect of neoadjuvant chemotherapy, and demonstrates that the SLUG-MMP3 axis could serve as a target for improving the efficacy of chemotherapy.

2020-12-11 | GSE163002 | GEO

Effect of systemic depletion of glutamine via PEGylated glutaminase on CT26 tumor tissue.

Project description:Proliferating cancer cells are addicted to glutamine for biomass synthesis and energy generation. We here enzymatically deplete circulating glutamine in mice and report how cancer cells adapt to low circulating glutamine and document immunological changes in the tumor microenvironment (TME) upon glutamine depletion in CT26 tumor model. We show that cancer cells adapt to low glutamine by diverting intracellular glutamine flux to nucleotide synthesis and downregulating global translation. Through immune cell deconvolution and GSEA, we show that systemic glutamine depletion is immunsosuppressive and marked by accumulaton of PMN-MDSC in the TME.

2024-04-16 | GSE247472 | GEO

Slug-induced miR-137 expression contributes to non-small cell lung cancer progression

Project description:The epithelial-mesenchymal transition (EMT) regulator Slug has multifaceted roles in controlling lung cancer progression, but the downstream targets and underlying mechanisms of Slug remain undetermined. The miRNAs downstream of Slug in lung cancer cells were examined using Illumina bead arrays and TaqMan low-density arrays.

2017-01-01 | GSE84040 | GEO

The invasion promoter Slug is a critical cell cycle regulator

Project description:Background: The well-characterized function of the transcriptional repressor, Slug, is to promote EMT and tumor invasion/metastasis by down-regulating E-cadherin expression. In this study, we investigated the significance of Slug during the S phase. Method: Slug mRNA expression was isolated from thymidine-arrested CL1-5/AS2neo (control) and CL1-5/AS2neo-Slug-WT stable cells. The Agilent oligonucleotide microarray analysis was performed to identify Slug downstream genes. Results: Overexpression of Slug inhibited lung [3H]-thymidine incorporation and delayed S phase progression. By using Agilent microarray we have identified panel of genes altered by Slug overexpression. Slug can down-regulate target genes about cell cycle networks for DNA replication, DNA replication checkpoint and genomic stability, such as TOP1, ORC4, RFC3, and Rad17. Conclusions: the multifaceted role of Slug in cancer progression by controlling the epithelial-mesenchymal transition and genome stability.

2012-02-09 | GSE35617 | GEO

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