deP domain containing 1 (dePdc1) and forkhead box transcription factor 3a (FoXo3a) serve a role in tumor cells. To the best of our knowledge, however, the expression of dePdc1 and FoXo3a in nephroblastoma and their role and potential mechanisms in nephroblastoma cells have not been reported. The aim of the present study was to characterize the expression of dePdc1 and FoXo3a in nephroblastoma, as well as the underlying mechanisms. The expression levels of dePdc1 and FoXo3a were detected using reverse transcription-quantitative Pcr and western blotting. cell viability, proliferation, invasion and migration were detected using cell counting Kit-8, colony formation, Transwell and wound healing assays, respectively. The activity of dePdc1 promoter was detected by dual-luciferase reporter assay and the association between FoXo3a and dePdc1 was detected using immunoprecipitation. dePdc1 expression was significantly increased in nephroblastoma cells, particularly WiT49 cells. compared with the negative control, dePdc1 knockdown significantly inhibited proliferation, invasion and migration of WiT49 cells, while dePdc1 overexpression (ov) reversed these effects. By contrast, expression of FoXo3a was decreased in WiT49 cells and immunoprecipitation showed that FoXo3a bound to the dePdc1 promoter. ov-FoXo3a inhibited WiT49 cell proliferation, invasion and migration, as well as protein expression levels of phosphorylated-glycogen synthase kinase-3β, Wnt3a and β-catenin, while dePdc1 ov reversed the inhibitory effects of FoXo3a ov on WiT49 cells. in conclusion, dePdc1 promoted malignant progression of nephroblastoma via the Wnt/β-catenin signaling pathway; this may be regulated by FoXo3a.
Background
C‐Jun N‐terminal kinase pathway‐associated phosphatase (JKAP) modulates the T cell receptor and mitogen‐activated protein kinase pathway‐mediated autoimmunity, thus participating in the pathogenesis of autoimmune diseases. This study aimed to explore the clinical implication of JKAP in inflammatory bowel disease (IBD) children.
Methods
C‐Jun N‐terminal kinase pathway‐associated phosphatase, tumor necrosis factor‐α (TNF‐α), interleukin‐23, interferon‐γ (T‐helper 1 secreted cytokine), and interleukin‐17A (T‐helper 17 secreted cytokine) in serum samples from 140 IBD children (including 60 Crohn's disease (CD) children and 80 ulcerative colitis (UC) children) were detected by ELISA. Meanwhile, JKAP from serum samples of 10 healthy controls (HCs) was also detected by ELISA.
Results
C‐Jun N‐terminal kinase pathway‐associated phosphatase was reduced in CD children (median (interquartile range (IQR)): 51.6 (36.8–69.5) pg/ml) and UC children (median (IQR): 57.5 (43.4–78.5) pg/ml) compared with HCs (median (IQR): 101.8 (70.0–143.2) pg/ml) (both
p
< 0.05). In CD children, JKAP was negatively correlated with C‐reactive protein (CRP) (
p
= 0.016) and erythrocyte sedimentation rate (ESR) (
p
= 0.029); while in UC children, JKAP was also negatively correlated with CRP (
p
= 0.006) and ESR (
p
= 0.022). Regarding the correlation of JKAP with disease activity, it presented negative correlations with PCDAI (
p
= 0.001) and PUCAI (
p
= 0.002). Besides, JKAP was negatively related to TNF‐α (both
p
< 0.05) but not interleukin‐23 (both
p
>0.05) in CD and UC children. Additionally, JKAP was not correlated with interferon‐γ in CD or UC children (both
p
>0.05), while negatively correlated with interleukin‐17A in CD and UC children (both
p
< 0.05).
Conclusion
C‐Jun N‐terminal kinase pathway‐associated phosphatase shows low expression and negative correlations with inflammation, disease activity, and T‐helper 17 cells in IBD children.
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