Search results for "HDAC3"
showing 4 items of 4 documents
Histone deacetylase inhibition by suberoylanilide hydroxamic acid: a therapeutic approach to treat human uterine leiomyoma.
2022
Objective To evaluate the effect of inhibition of histone deacetylases (HDACs) by suberoylanilide hydroxamic acid (SAHA) treatment of human uterine leiomyoma primary (HULP) cells in vitro on cell proliferation, cell cycle, extracellular matrix (ECM) formation, and transforming growth factor β3 (TGF-β3) signaling. Design Prospective study comparing uterine leiomyoma (UL) vs. adjacent myometrium (MM) tissue and cells with or without SAHA treatment. Setting Hospital and university laboratories. Patient(s) Women with UL without any hormone treatment. Intervention(s) Myomectomy or hysterectomy surgery in women for leiomyoma disease. Main Outcome Measure(s) HDAC activity was assessed by enzyme-li…
Deregulated repression of c-Jun provides a potential link to its role in tumorigenesis.
2004
The transcription factor c-Jun cooperates with oncogenic alleles of ras in malignant transformation. Constitutively active Ras causes, via activation of mitogen activated protein kinases, phosphorylation of c-Jun which is essential for subsequent target gene activation and tumorigenesis. Studying the mechanisms controlling c-Jun activity we found that its transcription activation function is actively repressed by a presumably multimeric repressor complex that includes histone deacetylase 3 as a critical subunit. Suppression of c-Jun is relieved by MAP kinase-mediated phosphorylation and/or titration of inhibitor components. The viral tumorigenic counterpart of c-Jun, v-Jun, escapes this inh…
JNK phosphorylation relieves HDAC3-dependent suppression of the transcriptional activity of c-Jun
2003
The AP-1 transcription factor c-Jun is a prototypical nuclear effector of the JNK signal transduction pathway. The integrity of JNK phosphorylation sites at serines 63/73 and at threonines 91/93 in c-Jun is essential for signal-dependent target gene activation. We show that c-Jun phosphorylation mediates dissociation of an inhibitory complex, which is associated with histone deacetylase 3 (HDAC3). The subsequent events that ultimately cause increased mRNA synthesis are independent of c-Jun phosphorylation and its interaction with JNK. These findings provide an 'activation by de-repression' model as an explanation for the stimulatory function of JNK on c-Jun.
Carbocysteine reverses the effects of cigarette smoke and improves the effects of beclomethasone on the histone deacetylases in bronchial epithelial …
2015
Cigarette smoke exposure, increasing oxidative stress, may negatively affect histone deacetylase expression/activity. Histone deacetylase expression/activity and in particular HDAC2, HDAC3, and SIRT-1 may control inflammation, cell senescence and responses to corticosteroids. The effects of carbocysteine and of beclomethasone on the histone deacetylase expression/activity in human bronchial epithelial cells stimulated with cigarette smoke extracts (CSE) are largely unknown. This study was aimed to explore whether carbocysteine and beclomethasone, in a bronchial epithelial cell line (16-HBE) exposed to CSE, were able to modulate the expression/activity of HDAC2, HDAC3, and of SIRT-1. Methods…