|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Consistent with this, PTGES knockdown also reduced the expression of CSC markers, tumor sphere formation, colony forming activity, tumorigenicity, and lung metastasis in vivo.
|
31285948 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
MiR-574-5p induces microsomal prostaglandin E synthase-1 (mPGES-1) expression by preventing CUGBP1 binding to its 3'UTR, leading to an enhanced alternative splicing and generation of an mPGES-1 3'UTR isoform, increased mPGES-1 protein expression, PGE<sub>2</sub> formation, and tumor growth <i>in vivo.</i> miR-574-5p-induced tumor growth in mice could be completely inhibited with the mPGES-1 inhibitor CIII.
|
30922080 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Immunohistochemical analyses showed the immunoreactivities of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 in tumor keratinocytes and stronger immunoreactivities of cyclooxygenase-2 and hematopoietic prostaglandin D synthase in epidermal dendritic cells (Langerhans cells).
|
29610553 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
By specifically targeting microsomal prostaglandin E synthase-1 (mPGES-1) activity with a small molecule inhibitor we could block CAF-derived PGE<sub>2</sub> production leading to reduced tumor growth, impaired angiogenesis, inhibited CAF migration and infiltration, reduced tumor cell proliferation and a favorable shift in the M1/M2 macrophage ratio.
|
29804818 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Tumor-infiltrating PD-L1<sup>+</sup> cells isolated from tumor-bearing mice also exerted morphology of tumor-associated macrophages and expressed high levels of prostaglandin E<sub>2</sub> (PGE<sub>2</sub>)-forming enzymes microsomal PGE<sub>2</sub> synthase 1 (mPGES1) and COX2.
|
28096371 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In conclusion, we propose that the initial event leading to tumor stem-cell activation may be a leveraged intrinsic mechanism in which all players are either inherent constituents (EGF) or highly inducible proteins (mPGES-1, iNOS) of tumor cells.
|
28257996 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Pharmacological inhibition of mPGES-1 and 5-LOX in M2 macrophages with specific inhibitor YS-121 in KPT-CD1d<sup>-/-</sup> mice decreased PanIN lesions and suppressed tumour growth in association with elevated levels of active CD8a cells.
|
28419443 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Mir-186 mimic inhibited VEGF expression in mPGES-1+/+ tumor xenografts and reduced tumor growth.
|
27322147 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We propose mPGES-1 as a possible new marker of tumour aggressiveness in PCa.
|
26113609 |
2015 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Moreover, using immunodeficient mice, we also demonstrated that both COX2- and mPGES1-overexpressing carcinoma cells were more efficient forming tumors.Our results describe for the first time the molecular pathway correlating PTGS2 and PTGES in colon cancer progression.
|
26498686 |
2015 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Investigation of the tumor microenvironment showed high infiltration of tumor-promoting macrophages with high expression of the M2-polarization markers CD163 and CD206. mPGES-1-expressing cells in tumors from different subtypes of neuroblastoma showed differential expression of one or several cancer-associated fibroblast markers such as vimentin, fibroblast activation protein α, α smooth muscle actin, and PDGF receptor β.
|
26080408 |
2015 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Moreover, mPGES-1 is often overexpressed in human colorectal tumors, and is thought to contribute to progression of these tumors.
|
25817443 |
2015 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Necrosis in DU145 prostate cancer spheroids induces COX-2/mPGES-1-derived PGE2 to promote tumor growth and to inhibit T cell activation.
|
23536473 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Consistent with these findings, we observed a significant reduction in multiplicity of tumors ≥1mm in diameter, suggesting that mPGES-1 contributes to mammary tumor growth.
|
23624019 |
2013 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Additionally, inhibiting the EGFR in mice bearing the A431 tumor, the mPGES-1 expression and the tumor growth, exhibited a parallel decline.
|
22081067 |
2012 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In a mouse tumor xenograft model, mPGES-1-overexpressed cells formed palpable tumors at earlier time points and developed larger tumors when compared with the control (P<0.01); in contrast, mPGES-1 knockdown delayed tumor development and reduced tumor size (P<0.01).
|
21743491 |
2012 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These results underscore the potential of mPGES-1 inhibitors as agents capable of controlling tumor growth.
|
22815767 |
2012 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In SCID mice with tumor xenografts, mPGES-1 overexpression accelerated tumor formation and increased tumor weight (P<.01), whereas mPGES-1 knockdown delayed tumor formation and reduced tumor weight (P<.01). mPGES-1 inhibited the expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN), leading to activation of the epidermal growth factor/phosphoinositide 3-kinase/AKT/mammalian target of rapamycin signaling pathways in cholangiocarcinoma cells. mPGES-1-mediated inhibition of PTEN is regulated through blocking of early growth response-1 sumoylation and binding to the 5'-untranslated region of the PTEN gene.
|
21354147 |
2011 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The present work was conducted to evaluate the expression of PGE(2)-pathway-related enzymes in human microvascular endothelial cells (HMVEC) in culture and to test the hypothesis that the tumor cell-HMVEC cross talk could increase mPGES-1 expression in HMVEC.
|
21277871 |
2011 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The results suggest that MPGES-1 is an alternative therapeutic target for cancer cells and tumours that express this enzyme.
|
20497297 |
2010 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
MPGES-1 expression was not related to overall PGE2 content in tumor and colon tissue, but decreased significantly in normal tissue during indomethacin exposure.
|
20043083 |
2010 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Localization of COX-2 and mPGES-1 was very similar, and well-differentiated tumors showed stronger expression than poorly/moderately differentiated tumors.
|
20034753 |
2010 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Surprisingly, mPGES-1 mRNA and protein levels were upregulated upon induction of a wild type-APC carrying vector in HT29 colon cancer cells, and downregulated following siRNA silencing of APC in HCT-116 cells. mPGES-1 was overall enhanced in human colorectal tumor specimens versus corresponding non-tumor mucosa and, in accordance with data on HT29 and HCT116 cells, higher levels of mPGES-1 were observed among tumors carrying wild type versus mutant APC.
|
19035518 |
2009 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Prostaglandin E2 is the major prostaglandin product of COX-2/microsomal prostaglandin E synthase-1 enzymatic pathway in medullary interstitial cells, and concomitant expression of COX-2, microsomal prostaglandin E synthase-1, and prostaglandin E2 receptor on interstitial cell tumors implies the presence of an autocrine growth loop important in pathogenesis of these tumors.
|
18619641 |
2008 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The protein and messenger RNA of mPGES-1 were both expressed at higher levels in the tumor samples (P < .001 and P = .006, respectively).
|
16952028 |
2006 |