Enhancement of prostaglandin D2 production through cyclooxygenase-2 and lipocalin-type prostaglandin D synthase by upstream stimulatory factor 1 in human brain-derived TE671 cells under serum starvation

Fujimori, Ko; Aritake, Kosuke; Urade, Yoshihiro

doi:10.1016/j.gene.2008.08.023

Cited by 6 publications

(8 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In both cases, the fluorescence intensity was decreased by the addition of 13-cis-retinoic acid in a concentration-dependent manner to Ͻ10% in the presence of 10 M 13-cis-retinoic acid, giving the same fluorescence quenching curves even in the presence of 10 M AT-56. These results indicate that AT-56 binds near Trp 54 in the AB-loop of L-PGDS but not to the Trp 43 residue in the retinoid-binding pocket, being consistent with the results obtained by NMR titration analysis.…”

Section: L-pgds Inhibitor At-56supporting

confidence: 91%

See 1 more Smart Citation

Biochemical, Functional, and Pharmacological Characterization of AT-56, an Orally Active and Selective Inhibitor of Lipocalin-type Prostaglandin D Synthase

Irikura

Aritake

Nagata

et al. 2009

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

Section: L-pgds Inhibitor At-56supporting

confidence: 91%

“…Recently, we demonstrated that L-PGDS produced PGD 2 coupled with COX-2 in TE-671 cells (43). L-PGDS coupled to COX-2 may be more sensitive to AT-56 than L-PGDS itself.…”

Section: Discussionmentioning

confidence: 93%

Biochemical, Functional, and Pharmacological Characterization of AT-56, an Orally Active and Selective Inhibitor of Lipocalin-type Prostaglandin D Synthase

Irikura

Aritake

Nagata

et al. 2009

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

“…Previous studies showed that the antiproliferative effects of γ -tocotrienol in combination with celecoxib, a COX-2 inhibitor, was associated with decreased expression of COX-2 and PGE 2 synthesis [22, 23]. Furthermore, COX-2 inhibition has been associated with decreased PGDS expression and PGD 2 synthesis [47]. Results in the present study show that combined treatment of γ -tocotrienol with PPAR γ antagonist decreased the protein and mRNA levels of COX-2 and PGDS, as well as decreased PGD 2 synthesis in +SA mammary tumor cells.…”

Section: Discussionmentioning

confidence: 99%

Synergistic Antiproliferative Effects of Combinedγ-Tocotrienol and PPARγAntagonist Treatment Are Mediated through PPARγ-Independent Mechanisms in Breast Cancer Cells

Malaviya

Sylvester

2014

PPAR Research

View full text Add to dashboard Cite

Previous findings showed that the anticancer effects of combined γ-tocotrienol and peroxisome proliferator activated receptor γ (PPARγ) antagonist treatment caused a large reduction in PPARγ expression. However, other studies suggest that the antiproliferative effects of γ-tocotrienol and/or PPARγ antagonists are mediated, at least in part, through PPARγ-independent mechanism(s). Studies were conducted to characterize the role of PPARγ in mediating the effects of combined treatment of γ-tocotrienol with PPARγ agonists or antagonists on the growth of PPARγ negative +SA mammary cells and PPARγ-positive and PPARγ-silenced MCF-7 and MDA-MB-231 breast cancer cells. Combined treatment of γ-tocotrienol with PPARγ antagonist decreased, while combined treatment of γ-tocotrienol with PPARγ agonist increased, growth of all cancer cells. However, treatment with high doses of 15d-PGJ2, an endogenous natural ligand for PPARγ, had no effect on cancer cell growth. Western blot and qRT-PCR studies showed that the growth inhibitory effects of combined γ-tocotrienol and PPARγ antagonist treatment decreased cyclooxygenase (COX-2), prostaglandin synthase (PGDS), and prostaglandin D2 (PGD2) synthesis. In conclusion, the anticancer effects of combined γ-tocotrienol and PPARγ antagonists treatment in PPARγ negative/silenced breast cancer cells are mediated through PPARγ-independent mechanisms that are associated with a downregulation in COX-2, PGDS, and PGD2 synthesis.

show abstract

“…Notably, four of the top-ranking factors ( USF1 , NFκB , ETS1 and MYC ) have already been shown to be involved in responses to serum starvation. For instance, this treatment enhanced USF1 expression and binding of USF1 in the promoter of the target gene lipocalin-type PGD synthase in brain-derived cells (54). NFκB has been found potently activated upon serum starvation in HEK293 cells, leading to apoptosis (32).…”

Section: Discussionmentioning

confidence: 99%

Functional analysis and identification of cis-regulatory elements of human chromosome 21 gene promoters

Warnatz¹,

Querfurth²,

Guerasimova³

et al. 2010

Nucleic Acids Research

View full text Add to dashboard Cite

Given the inherent limitations of in silico studies relying solely on DNA sequence analysis, the functional characterization of mammalian promoters and associated cis-regulatory elements requires experimental support, which demands cloning and analysis of putative promoter regions. Focusing on human chromosome 21, we cloned 182 gene promoters of 2500 bp in length and conducted reporter gene assays on transfected-cell arrays. We found 56 promoters that were active in HEK293 cells, while another 49 promoters could be activated by treatment of cells with Trichostatin A or depletion of serum. We observed high correlations between promoter activities and endogenous transcript levels, RNA polymerase II occupancy, CpG islands and core promoter elements. Truncation of a subset of 62 promoters to ∼500 bp revealed that truncation rarely resulted in loss of activity, but rather in loss of responses to external stimuli, suggesting the presence of cis-regulatory response elements within distal promoter regions. In these regions, we found a strong enrichment of transcription factor binding sites that could potentially activate gene expression in the presence of stimuli. This study illustrates the modular functional architecture of chromosome 21 promoters and helps to reveal the complex mechanisms governing transcriptional regulation.

show abstract

Enhancement of prostaglandin D2 production through cyclooxygenase-2 and lipocalin-type prostaglandin D synthase by upstream stimulatory factor 1 in human brain-derived TE671 cells under serum starvation

Cited by 6 publications

References 44 publications

Biochemical, Functional, and Pharmacological Characterization of AT-56, an Orally Active and Selective Inhibitor of Lipocalin-type Prostaglandin D Synthase

Biochemical, Functional, and Pharmacological Characterization of AT-56, an Orally Active and Selective Inhibitor of Lipocalin-type Prostaglandin D Synthase

Synergistic Antiproliferative Effects of Combinedγ-Tocotrienol and PPARγAntagonist Treatment Are Mediated through PPARγ-Independent Mechanisms in Breast Cancer Cells

Functional analysis and identification of cis-regulatory elements of human chromosome 21 gene promoters

Contact Info

Product

Resources

About