Sodium butyrate-induced autophagy in colorectal cancer unveils the Ca²⁺/CaMKKβ signaling pathway as a potential therapeutic target
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PROVIDER: PRJEB91763 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of colorectal cancer (CRC) cell line HT-29 treated with Sodium Butyrate. Sodium Butyrate, a HDAC inhibitor present in gut, can differentiate the undifferentiated HT-29 to enterocytes by the induction of brush border enzyme alkaline phosphatase. Results provide the transcriptional profiling underlying the butyrate-induced differentiation of CRC.
2016-12-31 | GSE61429 | GEO
Project description:As a histone deacetylase inhibitor, sodium butyrate and its derivative sodium phenylbutyrate involve in cellular events such as proliferation, differentiation, apoptosis and cell cycle control via reprogramming gene expression. However, the gene associated with the cell cycle control and molecular signaling triggering cell apopotosis and death are not well elucidated. Here, we treated A549 cells,a cell line belong to the non-small cells lung cancer,with high concentration of sodium butyrate or sodium phenylbutyrate and then used microarray identified differentially-expressed mRNA during this process.
2017-06-10 | GSE86928 | GEO
Project description:We analyzed a role of histone deacetylases in alternative splicing regulation. Using human exon arrays we identified a list of 683 genes whose splicing changes after HDAC inhibition with sodium butyrate. 6 samples (3 nontreated controls and 3 sodium butyrate treated cells)
2011-02-03 | E-GEOD-17397 | biostudies-arrayexpress
Project description:Promoting rumen development is closely related to the health and efficient growth of ruminants. We investigated the effect of sodium butyrate (SB) on rumen epithelium (RE), and whether the YAP1/TAZ-dependent alteration was involved in the RE developmental process induced by sodium butyrate. In the SB-treated cells, theYAP1/TAZ-dependent changes were not observed. SB increased the expression of genes involved in short-chain fatty acid (SCFA) metabolism, while YAP1/TAZ did not. Thus, SB mediated RE development was not associated with YAP1/TAZ.
2024-04-03 | GSE252749 | GEO
Project description:Machado-Joseph disease (MJD) is a fatal neurodegenerative disease caused by expansion of the trinucleotide repeat region within the ATXN3/MJD gene. Mutation of ATXN3 causes formation of neurotoxic ataxin-3 protein aggregates, neurodegeneration and motor deficits. Here we investigated the therapeutic potential and mechanistic activity of sodium butyrate (SB), the sodium salt of butyric acid, a metabolite naturally produced by gut microbiota, on cultured SH-SY5Y cells and transgenic zebrafish expressing human ataxin-3 containing 84 glutamine (Q) residues to model MJD. MJD SH-SY5Y cells were found to contain ataxin-3 oligomeric species and protein aggregates. Treatment with SB increased activity of the autophagy protein quality control pathway in the MJD cells, decreased presence of ataxin-3 aggregates and presence of ataxin-3 oligomers in an autophagy-dependent manner. Treatment with SB was also beneficial in vivo, improving swimming performance, increasing autophagy activity and decreasing presence of insoluble ataxin-3 protein species in the transgenic MJD zebrafish. Co-treating the MJD zebrafish with SB and chloroquine, an autophagy inhibitor, prevented the beneficial effects of SB on the zebrafish swimming, suggesting that the improved swimming performance was autophagy-dependent. To identify mechanism of the induction of autophagy by SB, we performed proteomic analysis of protein lysates from the SB treated and untreated MJD SH-SY5Y cells. We found that SB treatment had increased activity of Protein Kinase A and AMPK signaling. Immunoblot analysis confirmed that SB treatment had increased levels of acetylated FOXO1 protein. Further, co-treatment with an inhibitor of FOXO1 transcriptional activity (AS1842856) prevented the increase in autophagosome formation (LC3II/I) usually produced by SB treatment. Together our findings indicate that treatment with SB can increase activity of the autophagy pathway through a FOXO1-dependent process and that this has beneficial effects in vitro and in vivo. We propose that treatment with sodium butyrate warrants further investigation for the treatment of neurodegenerative diseases underpinned by proteinopathy mechanisms, including MJD.
2024-01-24 | PXD024626 | Pride
Project description:We analyzed a role of histone deacetylases in alternative splicing regulation. Using human exon arrays we identified a list of 683 genes whose splicing changes after HDAC inhibition with sodium butyrate.
2011-02-03 | GSE17397 | GEO
Project description:We performed global scale microarray analysis to identify detailed mechanisms by which sodium butyrate (SB) induce cell growth arrest and differentiation of colonic epithelial cells by using an Affymetrix GeneChip system. Colonic epithelial MCE301 cells used in this study were derived from transgenic mice harboring a tsSV40 large T-antigen. Arrested cell growth and a differentiated phenotype accompanying elevations of alkaline phosphatase activity and histone acetylation were observed in the cells treated with 2 mM SB. Of the 22,690 probe sets analyzed, approximately 2,000 genes were down- and up-regulated by a factor of 2.0 or greater in the cells treated with SB. Keywords: sodium butyrate, gene expression, colonic epithelial cell
2006-03-10 | GSE4410 | GEO
Project description:As a histone deacetylase inhibitor, sodium butyrate involves in cellular events such as proliferation, differentiation,apoptosis and cell cycle control via reprogramming gene expression. However, the target genes associated with the cell cycle control and molecular signaling triggering cell apopotosis and death are not well elucidated.
2016-12-29 | GSE58571 | GEO
Project description:The Madin-Darby bovine kidney epithelial cells, when at approximately 50% confluence (during the exponential phase), were treated with 10mM sodium butyrate for 24h. Butyrate induced profound changes in gene expression related with multiple signal transduction pathways such as cell cycle control, apoptosis and extracellular matrix remodeling in this cell line Keywords: stress response, two class unpaired design
2006-01-05 | GSE3970 | GEO
Project description:Sodium butyrate and bufexamac treatment of activated CD4+ T cells impairs de novo HIV-1 infection. RNAseq was used to obtain information about the cellular changes upon treatment, which could explain the observed effects on HIV-1 infection
2021-03-11 | GSE146854 | GEO