scholarly journals Rescue of human RET gene expression by sodium butyrate: a novel powerful tool for molecular studies in Hirschsprung disease

Gut ◽  
2003 ◽  
Vol 52 (8) ◽  
pp. 1154-1158 ◽  
Author(s):  
P Griseri
Keyword(s):  
Gene Expression ◽  
Sodium Butyrate ◽  
Hirschsprung Disease ◽  
Ret Gene ◽  
Molecular Studies

Effect of 5'-fluoro-2'-deoxycytidine and sodium butyrate on the genes of the intrinsic apoptotic pathway, p21, p53, cell viability, and apoptosis in human hepatocellular carcinoma cell lines

2021 ◽  
Author(s):  
Masumeh Sanaei ◽  
Fraidoon Kavoosi ◽  
Mohammad Amin Moezzi
Keyword(s):  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Cell Viability ◽  
Cell Lines ◽  
Sodium Butyrate ◽  
Cell Apoptosis ◽  
Chromatin Organization ◽  
Expression Level ◽  
Intrinsic Apoptotic Pathway ◽  
Apoptotic Pathway

Backgrounds: Epigenetic regulation such as DNA methylation plays a major role in chromatin organization and gene transcription. Additionally, histone modification is an epigenetic regulator of chromatin structure and influences chromatin organization and gene expression. The relationship between DNA methyltransferase (DNMTs) expression and promoter methylation of the tumor suppressor genes (TSGs) has been reported in various cancers. Previously, the effect of 5-aza-2'-deoxycytidine (5-AZA-CdR), trichostatin A (TSA), and valproic acid (VPA) was shown on various cancers. This study aimed to investigate the effect of 5'-fluoro-2'-deoxycytidine (FdCyd) and sodium butyrate on the genes of the intrinsic apoptotic pathway, p21, p53, cell viability, and apoptosis in human hepatocellular carcinoma SNU449, SNU475, and SNU368 cell lines. Materials and Methods: In this lab trial study, the SNU449, SNU475, and SNU368 cells were cultured and treated with 5'-fluoro-2'-deoxycytidine and sodium butyrate. To determine cell viability, cell apoptosis, and the relative gene expression level, MTT assay, flow cytometry assay, and qRT-PCR were done respectively. Results: 5'-fluoro-2'-deoxycytidine and sodium butyrate changed the expression level of the BAX, BAK, APAF1, Bcl-2, Bcl-xL, p21, and p53 gene (P<0.0001) by which induced cell apoptosis and inhibit cell growth in all three cell lines, SNU449, SNU475, and SNU368.  Conclusion: Both compounds played their roles through the intrinsic apoptotic pathway to induce cell apoptosis.

scholarly journals “Too much guts and not enough brains”: (epi)genetic mechanisms and future therapies of Hirschsprung disease — a review

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Emilie G. Jaroy ◽  
Lourdes Acosta-Jimenez ◽  
Ryo Hotta ◽  
Allan M. Goldstein ◽  
Ragnhild Emblem ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nervous System ◽  
Enteric Nervous System ◽  
Hirschsprung's Disease ◽  
Hirschsprung’S Disease ◽  
Current Knowledge ◽  
Hirschsprung Disease ◽  
Gut Development ◽  
Dna And Rna ◽  
Expression Of Genes

Abstract Hirschsprung disease is a neurocristopathy, characterized by aganglionosis in the distal bowel. It is caused by failure of the enteric nervous system progenitors to migrate, proliferate, and differentiate in the gut. Development of an enteric nervous system is a tightly regulated process. Both the neural crest cells and the surrounding environment are regulated by different genes, signaling pathways, and morphogens. For this process to be successful, the timing of gene expression is crucial. Hence, alterations in expression of genes specific for the enteric nervous system may contribute to the pathogenesis of Hirschsprung’s disease. Several epigenetic mechanisms contribute to regulate gene expression, such as modifications of DNA and RNA, histone modifications, and microRNAs. Here, we review the current knowledge of epigenetic and epitranscriptomic regulation in the development of the enteric nervous system and its potential significance for the pathogenesis of Hirschsprung’s disease. We also discuss possible future therapies and how targeting epigenetic and epitranscriptomic mechanisms may open new avenues for novel treatment.

Metabolic and gene expression hallmarks of seed germination uncovered by sodium butyrate in Medicago truncatula

2018 ◽  
Vol 42 (1) ◽  
pp. 259-269 ◽  
Author(s):  
Andrea Pagano ◽  
Susana de Sousa Araújo ◽  
Anca Macovei ◽  
Daniele Dondi ◽  
Simone Lazzaroni ◽  
...  
Keyword(s):  
Gene Expression ◽  
Seed Germination ◽  
Medicago Truncatula ◽  
Sodium Butyrate

scholarly journals Induction of carcinoembryonic-antigen-gene expression in human colorectal carcinoma by sodium butyrate

1990 ◽  
Vol 272 (2) ◽  
pp. 541-544 ◽  
Author(s):  
K Saini ◽  
G Steele ◽  
P Thomas
Keyword(s):  
Gene Expression ◽  
Colorectal Carcinoma ◽  
Carcinoembryonic Antigen ◽  
Sodium Butyrate ◽  
Blot Hybridization ◽  
Steady Increase ◽  
Dot Blot ◽  
Run Off ◽  
Cea Gene ◽  
Cea Mrna

The effect of sodium butyrate on the expression of the carcinoembryonic-antigen (CEA) gene was studied in two poorly differentiated colorectal-carcinoma cell lines (Clone-A and MIP-101) and in one well-differentiated cell line (LS-174T); A.T.C.C. no. CCL 188). Northern-blot and dot-blot analyses indicated a steady increase in CEA mRNA from day 4 to a maximal level by day 14 after these cells were exposed to 2 mM-sodium butyrate. Studies using nuclear run-off assays followed by dot-blot hybridization to a partial CEA cDNA clone demonstrated that specific increases in gene transcription rates (3-fold in MIP-101, 4-fold in LS-174T and 6-fold in Clone-A) are not sufficient to account for the observed increases in CEA mRNA abundance. Further studies showed that CEA-specific transcripts have a half-life of about 60-80 min, and treatment with sodium butyrate increased the stability of CEA-specific transcripts to about 340 min in LS-174T cells and to about 500 min in Clone-A cells. We conclude that the induction of the CEA-gene expression by sodium butyrate in colorectal-cancer cells is mediated by both transcriptional and post-transcriptional mechanisms, with CEA mRNA stability as one of the major check-points.

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