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Propionate reinforces epithelial identity and reduces aggressiveness of non-small cell lung carcinoma via chromatin remodelling [RNA-seq]

ABSTRACT: Propionate reinforces epithelial identity and reduces aggressiveness of non-small cell lung carcinoma via chromatin remodelling [RNA-seq]

PROVIDER: PRJNA934530 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23362162_1.fastq.gz	Fastqsanger.gz
	SRR23362162_2.fastq.gz	Fastqsanger.gz
	SRR23362163_1.fastq.gz	Fastqsanger.gz
	SRR23362163_2.fastq.gz	Fastqsanger.gz
	SRR23362164_1.fastq.gz	Fastqsanger.gz

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Propionate reinforces epithelial identity and reduces aggressiveness of non-small cell lung carcinoma via chromatin remodelling

Project description:Propionate reinforces epithelial identity and reduces aggressiveness of non-small cell lung carcinoma via chromatin remodelling

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Propionate reinforces epithelial identity and reduces aggressiveness of non-small cell lung carcinoma via chromatin remodelling [ChIP-seq]

Project description:Propionate reinforces epithelial identity and reduces aggressiveness of non-small cell lung carcinoma via chromatin remodelling [ChIP-seq]

| PRJNA932327 | ENA

Propionate reinforces epithelial identity and reduces aggressiveness of non-small cell lung carcinoma via chromatin remodelling [ChIP-seq]

Project description:To investigate the effect of sodium propionate (SP) in enhancing the epithelial gene program via epigenetic remodelling in NSCLC, A549 cell line was treated with SP for 3 hours. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) was performed for the histone mark H3K27ac in A549 cell line treated with SP for 3 hours.

2023-02-15 | GSE224739 | GEO

Propionate reinforces epithelial identity and reduces aggressiveness of non-small cell lung carcinoma via chromatin remodelling [RNA-seq]

Project description:To investigate the effect of sodium propionate (SP) in enhancing the epithelial gene program in NSCLC, lung cancer cells were treated with SP at different time points. Gene expression profiling using RNA-Seq then performed with A549 cells treated with SP at different time points (3 hours, 24 hours, 3 days and 12 days).

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Propionate reinforces epithelial identity and reduces aggressiveness of lung carcinoma.

Project description:The epithelial-to-mesenchymal transition (EMT) plays a central role in the development of cancer metastasis and resistance to chemotherapy. However, its pharmacological treatment remains challenging. Here, we used an EMT-focused integrative functional genomic approach and identified an inverse association between short-chain fatty acids (propionate and butanoate) and EMT in non-small cell lung cancer (NSCLC) patients. Remarkably, treatment with propionate in vitro reinforced the epithelial transcriptional program promoting cell-to-cell contact and cell adhesion, while reducing the aggressive and chemo-resistant EMT phenotype in lung cancer cell lines. Propionate treatment also decreased the metastatic potential and limited lymph node spread in both nude mice and a genetic NSCLC mouse model. Further analysis revealed that chromatin remodeling through H3K27 acetylation (mediated by p300) is the mechanism underlying the shift toward an epithelial state upon propionate treatment. The results suggest that propionate administration has therapeutic potential in reducing NSCLC aggressiveness and warrants further clinical testing.

| S-EPMC10701619 | biostudies-literature

Propionate reinforces epithelial identity and reduces aggressiveness of lung carcinoma

Project description:The epithelial-to-mesenchymal transition (EMT) plays a central role in the development of cancer metastasis and resistance to chemotherapy. However, its pharmacological treatment remains challenging. Here, we used an EMT-focused integrative functional genomic approach and identified an inverse association between short-chain fatty acids (propionate and butanoate) and EMT in non-small cell lung cancer (NSCLC) patients. Remarkably, treatment with propionate in vitro reinforced the epithelial transcriptional program promoting cell-to-cell contact and cell adhesion, while reducing the aggressive and chemo-resistant EMT phenotype in lung cancer cell lines. Propionate treatment also decreased the metastatic potential and limited lymph node spread in both nude mice and a genetic NSCLC mouse model. Further analysis revealed that chromatin remodelling through H3K27 acetylation (mediated by p300) is the mechanism underlying the shift towards an epithelial state upon propionate treatment. The results suggest that propionate administration has therapeutic potential in reducing NSCLC aggressiveness and warrants further clinical testing.

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Propionate reinforces epithelial identity and reduces aggressiveness of non-small cell lung carcinoma via chromatin remodelling

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

2023-02-15 | GSE224741 | GEO

Altered propionate metabolism contributes to tumor progression and aggressiveness

Project description:Altered propionate metabolism contributes to tumor progression and aggressiveness

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Altered propionate metabolism contributes to tumor progression and aggressiveness

Project description:The alteration of metabolic pathways is a critical strategy for cancer cells to attain the traits necessary for metastasis in disease progression. We found that dysregulation of propionate metabolism occurs through TGFbeta- and ERK2-driven downregulation of methylmalonyl-CoA epimerase (MCEE). MCEE downregulation occurs through a transcription factor Sp1/EGR1 switch at its promoter region, resulting in reduced flux through this anapleurotic pathway and leading to accumulation of methylmalonic acid (MMA), a byproduct of the propionate metabolism. MMA accumulation through alteration of propionate metabolism produces a pro-aggressive signature in breast and lung cancer cells and increases their metastatic potential. Altogether, we present a previously uncharacterized dysregulation of propionate metabolism as a novel contributor to cancer and a valuable potential target in the therapeutic treatment of metastatic carcinomas.

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Depletion of MALAT1-dependent WTAP reduces aggressiveness of hypoxic TNBC cells

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