Transcriptional activity analysis of promoter region of human PAX9 gene under dexamethasone, retinoic acid, and ergocalciferol treatment in MCF-7 and MDPC23

2010 ◽  
Vol 28 (7) ◽  
pp. 555-564 ◽  
Author(s):  
Liza L. Ramenzoni ◽  
Cristiane P.B. Saito ◽  
J. Justin McCormick ◽  
Sérgio R.P. Line
Keyword(s):  
Retinoic Acid ◽  
Promoter Region ◽  
Transcriptional Activity ◽  
Activity Analysis ◽  
Mcf 7

scholarly journals The Silencing Mediator of Retinoic Acid and Thyroid Hormone Receptor (SMRT) Corepressor Is Required for Full Estrogen Receptor α Transcriptional Activity

2007 ◽  
Vol 27 (17) ◽  
pp. 5933-5948 ◽  
Author(s):  
Theresa J. Peterson ◽  
Sudipan Karmakar ◽  
Margaret C. Pace ◽  
Tong Gao ◽  
Carolyn L. Smith
Keyword(s):  
Estrogen Receptor ◽  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Transcriptional Activity ◽  
Thyroid Hormone Receptor ◽  
Estrogen Receptor Α ◽  
Receptor Interaction ◽  
Positive Effects ◽  
Mcf 7

ABSTRACT Multiple factors influence estrogen receptor α (ERα) transcriptional activity. Current models suggest that the silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressor functions within a histone deactylase-containing protein complex that binds to antiestrogen-bound ERα and contributes to negative regulation of gene expression. In this report, we demonstrate that SMRT is required for full agonist-dependent ERα activation. Chromatin immunoprecipitation assays demonstrate that SMRT, like ERα and the SRC-3 coactivator, is recruited to an estrogen-responsive promoter in estrogen-treated MCF-7 cells. Depletion of SMRT, but not histone deacetylases 1 or 3, negatively impacts estradiol-stimulated ERα transcriptional activity, while exogenous expression of SMRT's receptor interaction domains blocks ERα activity, indicating a functional interaction between this corepressor and agonist-bound ERα. Stimulation of estradiol-induced ERα activity by SMRT overexpression occurred in HeLa and MCF-7 cells, but not HepG2 cells, indicating that these positive effects are cell type specific. Similarly, the ability of SMRT depletion to promote the agonist activity of tamoxifen was observed for HeLa but not MCF-7 cells. Furthermore, impairment of agonist-stimulated activity by SMRT depletion is specific to ERα and not observed for receptors for vitamin D, androgen, or thyroid hormone. Nuclear receptor corepressor (N-CoR) depletion increased the transcriptional activity of all four tested receptors. SMRT is required for full expression of the ERα target genes cyclin D1, BCL-2, and progesterone receptor but not pS2, and its depletion significantly attenuated estrogen-dependent proliferation of MCF-7 cells. Taken together, these data indicate that SMRT, in conjunction with gene-specific and cell-dependent factors, is required for positively regulating agonist-dependent ERα transcriptional activity.

scholarly journals Real-Time Challenging of ERα Y537S Mutant Transcriptional Activity in Living Cells

Endocrines ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 54-64
Author(s):  
Manuela Cipolletti ◽  
Sara Pescatori ◽  
Filippo Acconcia
Keyword(s):  
Cell Line ◽  
Transcriptional Activity ◽  
Estrogen Receptor Α ◽  
Living Cells ◽  
Patient Treatment ◽  
Estrogen Responsive Element ◽  
Specific Proteins ◽  
Responsive Element ◽  
Mcf 7

Metastatic estrogen receptor α (ERα)-expressing breast cancer (BC) occurs after prolonged patient treatment with endocrine therapy (ET) (e.g., aromatase inhibitors—AI; 4OH-tamoxifen—4OH-Tam). Often these metastatic BCs express a mutated ERα variant (e.g., Y537S), which is transcriptionally hyperactive, sustains uncontrolled proliferation, and renders tumor cells insensitive to ET drugs. Therefore, new molecules blocking hyperactive Y537S ERα mutation transcriptional activity are requested. Here we generated an MCF-7 cell line expressing the Y537S ERα mutation stably expressing an estrogen-responsive element (ERE) promoter, which activity can be monitored in living cells. Characterization of this cell line shows both hyperactive basal transcriptional activity with respect to normal MCF-7 cells, which stably express the same ERE-based promoter and a decreased effect of selective ER downregulators (SERDs) in reducing Y537S ERα mutant transcriptional activity with respect to wild type ERα transcriptional activity. Kinetic profiles of Y537S ERα mutant-based transcription produced by both drugs inducing receptor degradation and siRNA-mediated depletion of specific proteins (e.g., FOXA1 and caveolin1) reveals biphasic dynamics of the inhibition of the receptor-regulated transcriptional effects. Overall, we report a new model where to study the behavior of the Y537S ERα mutant that can be used for the identification of new targets and pathways regulating the Y537S ERα transcriptional activity.

scholarly journals Retinol and retinaldehyde specifically increase α1-proteinase inhibitor in the human cornea

1997 ◽  
Vol 322 (3) ◽  
pp. 751-756 ◽  
Author(s):  
Goran BOŠKOVIĆ ◽  
Sally S. TWINING
Keyword(s):  
Retinoic Acid ◽  
Proteinase Inhibitor ◽  
Culture Medium ◽  
Final Concentration ◽  
Maximal Response ◽  
Human Cornea ◽  
Hep G2 ◽  
Monocytes And Macrophages ◽  
Extrahepatic Tissues ◽  
Mcf 7

α1-Proteinase inhibitor is a serpin and can inhibit most serine proteinases. The cornea is one of several extrahepatic tissues that synthesizes this inhibitor. In the presence of retinol, corneal α1-proteinase inhibitor levels were increased 3.8-fold. The maximal response was achieved 2 h after the addition of retinol (1 μM final concentration) to the culture medium. A similar increase in α1-proteinase inhibitor was observed with retinaldehyde (1 nM final concentration). Concentrations of α1-proteinase inhibitor in other tested cells (Hep G2, CaCo 2, MCF-7, monocytes and macrophages) remained unchanged in the presence of retinol. Retinoic acid did not affect α1-proteinase inhibitor levels in the cornea or the other cells tested. The acute-phase cytokine, interleukin-6, increased α1-proteinase inhibitor levels in all tested tissues/cells except the cornea. These results demonstrate that α1-proteinase inhibitor levels are controlled differently in the cornea compared with other tissues/cells. α1-Proteinase inhibitor is the first protein identified whose levels are regulated by a mechanism supported by retinol and retinaldehyde but not retinoic acid.

scholarly journals Stemness marker ALDH1A1 promotes tumor angiogenesis via retinoic acid/HIF-1α/VEGF signalling in MCF-7 breast cancer cells

2018 ◽  
Vol 37 (1) ◽  
Author(s):  
Valerio Ciccone ◽  
Erika Terzuoli ◽  
Sandra Donnini ◽  
Antonio Giachetti ◽  
Lucia Morbidelli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Retinoic Acid ◽  
Cancer Cells ◽  
Tumor Angiogenesis ◽  
Breast Cancer Cells ◽  
Vegf Signalling ◽  
Mcf 7

VITAMIN D DERIVATIVES IN COMBINATION WITH 9-cis RETINOIC ACID PROMOTE ACTIVE CELL DEATH IN BREAST CANCER CELLS

1995 ◽  
Vol 14 (3) ◽  
pp. 391-394 ◽  
Author(s):  
S Y James ◽  
A G Mackay ◽  
K W Colston
Keyword(s):  
Breast Cancer ◽  
Vitamin D ◽  
Retinoic Acid ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
P53 Protein ◽  
Protein A ◽  
Therapeutic Implications ◽  
Protein Levels ◽  
Mcf 7

ABSTRACT The effects of the novel vitamin D analogue, EB1089 alone, or in combination with the retinoid, 9-cis retinoic acid (9-cis RA) on indices of apoptosis in MCF-7 breast cancer cells have been examined. EB1089 was capable of reducing bcl-2 protein, a suppressor of apoptosis, and increasing p53 protein levels in MCF-7 cell cultures following 96h treatment. In the presence of 9-cis RA, EB1089 acted to further enhance the down-regulation and up-regulation of bcl-2 and p53 respectively. Furthermore, EB1089 induces DNA fragmentation in MCF-7 cells, a key feature of apoptosis, alone and in combination with 9-cis RA in situ. The observation that EB1089 and 9-cis RA act in a cooperative manner to enhance induction of apoptosis in these cells may have therapeutic implications.

Transcriptional activity of icaADBC is not correlated to the degree of biofilm formation in clinical ica-positive Staphylococcus epidermidis strains

Biofilms ◽  
2004 ◽  
Vol 1 (2) ◽  
pp. 101-106 ◽  
Author(s):  
S. Dobinsky ◽  
H. Rohde ◽  
J. K.-M. Knobloch ◽  
M. A. Horstkotte ◽  
D. Mack
Keyword(s):  
Sequence Analysis ◽  
Growth Phase ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Promoter Region ◽  
Transcriptional Activity ◽  
Exponential Growth Phase ◽  
Polysaccharide Intercellular Adhesin ◽  
Different Strains ◽  
Negative Phenotype

Biofilm-formation in Staphylococcus epidermidis depends on the expression of the icaADBC operon encoding the enzymes required for the synthesis of polysaccharide intercellular adhesin (PIA). Different S. epidermidis strains vary widely in the degree of PIA and biofilm that they produce. In 11 clinical S. epidermidis strains we analyzed the biofilm-forming capacity in relation to the amount of ica expressed in static biofilm cultures. In mid-exponential growth phase no correlation could be detected between the level of ica transcription and the biofilm-forming phenotype. When the different strains were grown under conditions leading to a biofilm-negative phenotype, ica-expression was highly upregulated. Sequence analysis demonstrated that the observed differences were not due to major mutations in the ica promoter region but apparently to other strain-specific regulators.

Effects of retinoic acid isomers on proteomic pattern in human breast cancer MCF-7 cell line

2013 ◽  
Vol 47 (04) ◽  
pp. 205-209 ◽  
Author(s):  
D. Flodrova ◽  
D. Benkovska ◽  
D. Macejova ◽  
L. Bialesova ◽  
J. Bobalova ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Retinoic Acid ◽  
Cell Line ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Mcf 7

scholarly journals (Inverse) Agonists of Retinoic Acid–Related Orphan Receptor γ: Regulation of Immune Responses, Inflammation, and Autoimmune Disease

2020 ◽  
Vol 60 (1) ◽  
pp. 371-390 ◽  
Author(s):  
Anton M. Jetten ◽  
Donald N. Cook
Keyword(s):  
Retinoic Acid ◽  
Autoimmune Disease ◽  
Immune Responses ◽  
Autoimmune Diseases ◽  
Transcriptional Activity ◽  
Cholesterol Metabolism ◽  
Cholesterol Biosynthesis ◽  
Critical Role ◽  
Orphan Receptor ◽  
Inverse Agonists

Retinoic acid–related orphan receptor γt (RORγt) functions as a ligand-dependent transcription factor that regulates multiple proinflammatory genes and plays a critical role in several inflammatory and autoimmune diseases. Various endogenous and synthetic RORγ (inverse) agonists have been identified that regulate RORγ transcriptional activity, including many cholesterol intermediates and oxysterols. Changes in cholesterol biosynthesis and metabolism can therefore have a significant impact on the generation of oxysterol RORγ ligands and, consequently, can control RORγt activity and inflammation. These observations contribute to a growing literature that connects cholesterol metabolism to the regulation of immune responses and autoimmune disease. Loss of RORγ function in knockout mice and in mice treated with RORγ inverse agonists results in reduced production of proinflammatory cytokines, such as IL-17A/F, and increased resistance to autoimmune disease in several experimental rodent models. Thus, RORγt inverse agonists might provide an attractive therapeutic approach to treat a variety of autoimmune diseases.

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