Fig 1: Effects of testosterone on FBP1 mRNA expression in GCs. (A) Expression of FBP1 was significantly increased in GC streated with 1×10-6, 1×10-5, 1×10-4 and 1×10-3 mol/l testosterone compared with in the CTR group, *P<0.05 vs. CTR group. (B) FBP1 mRNA expression was significantly increased in GCs treated with testosterone for 2, 12 and 48 h compared with the CTR group at the same time. FBP1 mRNA expression was increased in GCs treated with flutamide + testosterone at 48 h compared with the CTR group. Treatment of GCs with flutamide led to a significant upregulation in FBP1 expression at 2, 24 and 48 h compared with the CTR group. Conversely, when treated with flutamide + testosterone, mRNA expression in GCs was significantly decreased at 12 and 24 h. *P<0.05 vs. respective CTR group. CTR, control group (no testosterone treatment); T, testosteronetreatment group; F, flutamide treatment group; F+T, flutamide + testosterone group; FBP1, fructose-1,6-bisphosphatase 1; GC, granulosa cell.
Fig 2: FBP1 suppresses epithelial-mesenchymal transition in gastric cancer.FBP1 expression was positively correlated with E-cadherin mRNA levels, and negatively correlated with N-cadherin expression in TCGA database (P<0.05). Over-expression of FBP1 resulted in increased expression of E-cadherin and decreased expression of Vimentin and N-cadherin both on protein level (A) and transcriptional level (B). (C) Confocal microscopy analysis of phenotypic marker including E-cadherin, crystal violet Vimentin. The red signal represents the staining of corresponding protein, and the blue signal represents the nuclear DNA staining by DAPI.
Fig 3: Kaplan-Meier estimates of the overall survival and disease free survival of gastric cancer patients with different expression levels of FBP1.The Kaplan-Meier plots were used to visualize the survival probabilities for high and low FBP1 expression in gastric patients. The tick marked on the Kaplan-Meier curves represents the censored subjects. The differences between the two curves were determined by the two-sided log-rank test. (A) overall survival, ?2 = 8.390, P = 0.004; (B) disease free survival, ?2 = 12.401, P<0.001.
Fig 4: A Summary of the Observed Metabolic States of Quiescent, LPS Stimulated, and COPD NeutrophilsA diagram showing the metabolic states of resting (A), stimulated (B), and COPD (C) neutrophils showing increased glycolytic activity and glycogen synthesis in response to LPS and defective glycogen cycling and glycolysis in COPD. Genes identified to actively regulate neutrophil glucose transport (Glut1), gluconeogenesis (GNG) (Fbp1 and Pck2), glycogenesis (Gys1, Gbe1, and Ugp2), and glycogenolysis (Pygl) are highlighted in red. Arrow thickness indicates the relative flux through metabolic pathways with glycogenolysis and glucose oxidation highlighted in blue and glycogenesis and gluconeogenesis in green.
Fig 5: Effects of testosterone and/or flutamide on the expression of FBP1 signaling pathway genes in GCs and TICs. (A) Testosterone induced a significant increase in the mRNA expression levels of FBP1 and PCK1 in GCs compared with the CTR group, whereas testosterone significantly inhibited FOXO1 and PGC-1a mRNA expression. *P<0.05 vs. respective CTR group. Flutamide promoted the expression of FOXO1, and inhibited the expression of FBP1 and PGC-1a mRNA in GCs compared with the CTR group. *P<0.05 vs. respective CTR group. (B) In TICs, testosterone or flutamide, or a combination of the two inhibited the mRNA expression of FOXO1 and G6PC compared with the CTR group, but promoted the mRNA expression of PCK1. *P<0.05 vs. respective CTR group. There was no significant effect on the expression of FBP1 mRNA in TIC by testosterone or fluoride, P>0.05. CTR, control group (no testosterone treatment); T, testosteronetreatment group; F, flutamide treatment group; F+T, flutamide + testosterone group; FOXO1, forkhead box protein O1; PGC-1a, peroxisome proliferator-activated receptor ? coactivator 1a; FBP1, fructose-1,6-bisphosphatase 1; PCK1, phosphoenolpyruvate carboxykinase 1; TIC, theca-interstitial cell; GC, granulosa cell; G6PC, glucose-6-phosphatase catalytic subunit.
Supplier Page from Abcam for Anti-FBP1 antibody [EPR4619]