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

ABSTRACT: 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).

ORGANISM(S): Homo sapiens

PROVIDER: GSE224740 | GEO | 2023/02/15

REPOSITORIES: GEO

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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 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.

| S-SCDT-10_15252-EMMM_202317836 | biostudies-other

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

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

| PRJNA932329 | ENA

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.

2022-01-28 | GSE161108 | GEO

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

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

| PRJNA934530 | ENA

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

Altered propionate metabolism contributes to tumor progression and aggressiveness

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

| PRJNA675592 | ENA

Investigation on the anaerobic propionate degradation by Escherichia coli K12

Project description:Propionate is an abundant carboxylic acid in nature. Microorganisms metabolize propionate aerobically via the 2-methylcitrate pathway. This pathway depends on a series of three reactions in the citric acid cycle that leads to the conversion of succinate to oxaloacetate. Interestingly, the gamma-proteobacterium Escherichia coli can use propionate as a carbon and electron source under oxic but not under anoxic conditions. The typical downregulation of the citric acid cycle under anoxic conditions is only partially responsible for the inability to use propionate under anoxic conditions since an arcA mutant shows very limited growth on propionate. RT-PCR and transcriptomic analysis revealed a post-transcriptional regulation of the prp-genecluster encoding the necessary enzymes for propionate metabolism. The polycistronic mRNA was hydrolyzed in the 3`-5` direction under anoxic conditions. This regulatory strategy is highly constructive because the last gene of the operon encodes the first enzyme of the propionate metabolism. Further analysis revealed that RNase R catalyzes the hydrolysis of the prp transcripts. Consequently, an rnr-deletion strain could metabolize propionate under anoxic conditions. To the best of our knowledge, this is the first study describing the influence of RNase R on the anaerobic metabolism of E. coli.

2017-12-14 | GSE78814 | GEO

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