A Novel Role of Sodium Butyrate in the Regulation of Cancer-associated Aromatase Promoters 1.3 and II by Disrupting a Transcriptional Complex in Breast Adipose Fibroblasts

2007 ◽  
Vol 2007 ◽  
pp. 23
Author(s):  
S.E. Bulun
Keyword(s):  
Sodium Butyrate ◽  
Breast Adipose ◽  
Transcriptional Complex

scholarly journals A Novel Role of Sodium Butyrate in the Regulation of Cancer-associated Aromatase Promoters I.3 and II by Disrupting a Transcriptional Complex in Breast Adipose Fibroblasts

2005 ◽  
Vol 281 (5) ◽  
pp. 2585-2597 ◽  
Author(s):  
Santanu Deb ◽  
Jianfeng Zhou ◽  
Sanober A. Amin ◽  
Ayse Gonca Imir ◽  
Mehmet Bertan Yilmaz ◽  
...  
Keyword(s):  
Sodium Butyrate ◽  
Breast Adipose ◽  
Transcriptional Complex

scholarly journals Obesity and Breast Cancer: The Role of Crown-Like Structures in Breast Adipose Tissue in Tumor Progression, Prognosis, and Therapy

2020 ◽  
Vol 23 (3) ◽  
pp. 233 ◽  
Author(s):  
Sara Socorro Faria ◽  
Luís Henrique Corrêa ◽  
Gabriella Simões Heyn ◽  
Lívia Pimentel de Sant'Ana ◽  
Raquel das Neves Almeida ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Tumor Progression ◽  
Breast Adipose Tissue ◽  
Breast Adipose

Role of thalidomide, senicapoc, and sodium butyrate in choroidal neovascularization

2020 ◽  
Vol 530 (2) ◽  
pp. 367-373
Author(s):  
Valeriy Lyzogubov ◽  
Michael Dasso ◽  
Nalini Bora ◽  
Puran S. Bora
Keyword(s):  
Choroidal Neovascularization ◽  
Sodium Butyrate

scholarly journals An indisputable role of NHE8 in mucosal protection

2020 ◽  
Vol 319 (4) ◽  
pp. G421-G431
Author(s):  
Claudio Bernardazzi ◽  
Hua Xu ◽  
Huan Tong ◽  
Daniel Laubitz ◽  
Vanessa Figliuolo da Paz ◽  
...  
Keyword(s):  
Cell Volume ◽  
Sodium Butyrate ◽  
Volume Regulation ◽  
Fecal Microbiota Transplantation ◽  
Cell Volume Regulation ◽  
Fecal Microbiota ◽  
Mucosal Protection ◽  
Ph Homeostasis ◽  
Mucin Production

Loss of Na+/H+ exchanger isoform 8 (NHE8), a Slc9 family of exchanger that contributes to sodium uptake, cell volume regulation, and intracellular pH homeostasis, resulted in dysbiosis with reduction of butyrate-producing bacteria and decrease of Muc2 production in the intestine in mice. Introducing fecal microbiota transplantation (FMT) and VSL#3 in NHE8 knockout (NHE8KO) mice failed to rebalance the microbiota in these mice. Furthermore, administration of FMT, VSL#3, and sodium butyrate was unable to restore mucin production in the absence of NHE8 in the intestine.

scholarly journals Sodium butyrate inhibits myogenesis by interfering with the transcriptional activation function of MyoD and myogenin.

1992 ◽  
Vol 12 (11) ◽  
pp. 5123-5130 ◽  
Author(s):  
L A Johnston ◽  
S J Tapscott ◽  
H Eisen
Keyword(s):  
Sodium Butyrate ◽  
Transcriptional Activation ◽  
Activation Function ◽  
Muscle Differentiation ◽  
Transcriptional Activators ◽  
Present Evidence ◽  
Dna Transcription ◽  
Basic Helix Loop Helix ◽  
Helix Loop Helix

Sodium butyrate reversibly inhibits muscle differentiation and blocks the expression of many muscle-specific genes in both proliferating myoblasts and differentiated myotubes. We investigated the role of the basic helix-loop-helix (bHLH) myogenic determinator proteins MyoD and myogenin in this inhibition. Our data suggest that both MyoD and myogenin are not able to function as transcriptional activators in the presence of butyrate, although both apparently retain the ability to bind DNA. Transcription of MyoD itself is extinguished in butyrate-treated myoblasts and myotubes, an effect that may be due to the inability of MyoD to autoactivate its own transcription. We present evidence that the HLH region of MyoD is essential for butyrate inhibition of MyoD. In contrast to MyoD and myogenin, butyrate does not inhibit the ubiquitous basic HLH protein E2-5 from functioning as a transcriptional activator.

p21Waf1 deficiency does not decrease DNA repair in E1A+cHa-Ras transformed cells by HDI sodium butyrate

2018 ◽  
Vol 399 (11) ◽  
pp. 1297-1304
Author(s):  
Maria Igotti ◽  
Olga Gnedina ◽  
Alisa Morshneva ◽  
Svetlana Svetlikova ◽  
Valery Pospelov
Keyword(s):  
Dna Repair ◽  
Sodium Butyrate ◽  
Inhibitory Effect ◽  
Genome Integrity ◽  
Transformed Cells ◽  
Wild Type ◽  
Γh2ax Foci ◽  
Deacetylase Inhibitor ◽  
Host Cell Reactivation

AbstractThis study aimed to explore a role of p21Waf1 in γH2AX foci formation and DNA repair as assessed by a Host-Cell Reactivation Assay in wild-type (p21Waf+/+) and p21Waf1-deficient E1A+Ras-transformed cells. p21Waf1+/+cells have low γH2AX background compared to p21Waf1−/−cells. The treatment with histone deacetylase inhibitor (HDI) sodium butyrate (NaBut) causes to accumulation of γH2AX in p21Waf+/+cells with little effect in p21Waf−/−cells. Moreover, NaBut inhibits DNA repair in wt cells but not in p21Waf1−/−cells. This could be explained by the weakening of GADD45 and PCNA proteins binding in NaBut-treated p21Waf1-expressing cells but not in p21Waf1−/−cells. We suggest that in wt-ERas cells NaBut activates both p21Waf1 expression and a release of p21Waf1 from the complexes with E1A that leads to suppression of DNA repair and promotes γH2AX persistency. The absence of p21Waf1 is by itself considered by the cell as stressful factor with formation of γH2AX. But the lack of p21Waf1 interferes with an inhibitory effect of NaBut to inhibit DNA repair and thereby to stop concomitant accumulation of harmful mutations. We conclude that p21Waf1 is directly involved in control of genome integrity and DNA repair acting through modulation of the components of the DNA repair machinery.

scholarly journals A polycomb-independent role of EZH2 in TGFβ1-damaged epithelium triggers a fibrotic cascade with mesenchymal cells

2020 ◽  
Author(s):  
Huy Quang Le ◽  
Matthew Alexander Hill ◽  
Ines Kollak ◽  
Wioletta Skronska-Wasek ◽  
Victoria Schroeder ◽  
...  
Keyword(s):  
Rna Polymerase Ii ◽  
Cell Fate ◽  
Transforming Growth Factor ◽  
Cell Types ◽  
Transforming Growth Factor Β1 ◽  
Therapeutic Interventions ◽  
Polycomb Repressive Complex 2 ◽  
Cell Fate Decisions ◽  
Transcriptional Complex

AbstractTo restore organ homeostasis, a myriad of cell types need to activate rapid and transient programs to adjust cell fate decisions and elicit a collective behaviour. Characterisation of such programs are imperative to elucidate an organ’s regenerative capacity and its aberrant repair in disease. By modelling epithelial-mesenchymal crosstalk, we provide direct evidence for transforming growth factor β1 (TGFβ1)-damaged epithelium initiating a bi-directional fibrotic cascade with the mesenchyme. Strikingly, TGFβ1-damaged epithelia facilitates the release of Enhancer of Zester Homolog 2 (EZH2) from Polycomb Repressive Complex 2 (PRC2) to establish a novel fibrotic transcriptional complex of EZH2, RNA-polymerase II (POL2) and nuclear actin. Perturbing this complex by disrupting epithelial EZH2 or actomyosin remodelling abrogates the fibrotic crosstalk. The liberation of EZH2 from PRC2 is accompanied by an EZH2-EZH1 switch to preserve global H3K27me3 occupancy. Our results reveal an important non-canonical function of EZH2, paving the way for therapeutic interventions in fibrotic disease.

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