Prostaglandin synthases influence thyroid follicular cell proliferation but not carcinogenesis in rats initiated with N-bis(2-hydroxypropyl)nitrosamine.
Prostaglandin synthases influence thyroid follicular cell proliferation but not carcinogenesis in rats initiated with N-bis(2-hydroxypropyl)nitrosamine.
Prostaglandin synthases influence thyroid follicular cell proliferation but not carcinogenesis in rats initiated with N-bis(2-hydroxypropyl)nitrosamine.
In a recent study, we found an association of the minor PTGES2Arg298His allele and lower risk of type 2 diabetes mellitus in the European Investigation into Cancer and Nutrition (EPIC) and Cooperative Health Research in the Augsburg Region (KORA) cohorts.
Stable PTGES2-shRNA transfectants were generated in Ishikawa and Hec-1B endometrial cancer cell lines, and transfection efficiencies were confirmed by RT-PCR and Western blot analyses.
Overall, our study shows that mPGES-2 can protect renal tubular epithelial cells by regulating autophagy levels and aggravation of acute kidney injury by mPGES-2 down regulation is associated with autophagy inhibition and enhanced apoptosis.
Stable PTGES2-shRNA transfectants were generated in Ishikawa and Hec-1B endometrial cancer cell lines, and transfection efficiencies were confirmed by RT-PCR and Western blot analyses.
The most predictive signature was achieved with interleukin 1β, MUC4, and prostaglandin E synthase 2 to accurately discriminate high-risk cysts from low-risk cysts with an area under the curve of up to 0.86 (p = 0.002).
The prostaglandin E synthase 2 (PTGES2) gene maps to a locus linked to obesity and is involved in the synthesis of the antilipolytic compound prostaglandin E(2).
The inflammatory mediator prostaglandin E(2) (PGE(2)) is implicated in the pathogenesis of chronic inflammatory diseases including periodontitis; it is synthesized by cyclooxygenases (COX) and the prostaglandin E synthases mPGES-1, mPGES-2, and cPGES.
Using tissue microarrays, the expression of COX-2, microsomal-PGES-1 and -PGES-2 (mPGES-1 and mPGES-2), as well as EGFR was evaluated in different subtypes of thymoma and thymic carcinomas.
The expression levels of eight enzymes (ALOX5, ALOX5AP, CYP2C8, CYP4F11, LTA4H, PLA2G4A, CYP2D6, PTGES2) correlated with the survival time of ESCC patients.
Among non-obese individuals, the GG genotype of PTGES2rs10987883 was associated with an increased risk for prostate cancer (unadjusted, recessive model OR = 3.23, 95% CI: 1.27-8.23).
Here, we employed our Metabolic Intervention Cohort Kiel (MICK) to assess the influence of the PTGES2Arg298His polymorphism on a wider scale of parameters of the metabolic syndrome and postprandial metabolism.
Among non-obese individuals, the GG genotype of PTGES2rs10987883 was associated with an increased risk for prostate cancer (unadjusted, recessive model OR = 3.23, 95% CI: 1.27-8.23).
The expression levels of eight enzymes (ALOX5, ALOX5AP, CYP2C8, CYP4F11, LTA4H, PLA2G4A, CYP2D6, PTGES2) correlated with the survival time of ESCC patients.
The PTGES2Arg298His polymorphism was reinvestigated in a population-based cross-sectional study (Cooperative Health Research in the Augsburg Region) consisting of 239 individuals with impaired glucose tolerance, 226 with type 2 diabetes, and 863 normoglycemic controls.