Fig 1: CSN3 is associated with activation of NOD1/RIP2/NF-κB-related inflammatory signaling in gastric cancer cells. (A) Western blot analysis of NOD1, RIP2, p-P65, and P65 protein expression in gastric cancer cells after CSN3 overexpression. GAPDH was used as the loading control. (B) Western blot analysis of NOD1, RIP2, p-P65, and P65 protein expression in gastric cancer cells after CSN3 knockdown. GAPDH was used as the loading control. (C) RT-qPCR analysis of IL-1β, IL-6, IL-8, and TNF-α mRNA expression in SGC-7901, BGC-823, and AGS cells following CSN3 overexpression. (D) RT-qPCR analysis of IL-1β, IL-6, IL-8, and TNF-α mRNA expression in SGC-7901, BGC-823, and AGS cells following CSN3 knockdown. *, P<0.05; **, P<0.01; ***, P<0.001. CSN3, casein kappa; IL, interleukin; NOD1, nucleotide-binding oligomerization domain-containing protein 1; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; TNF-α, tumor necrosis factor-alpha.
Fig 2: The effects of CSN3 overexpression on the proliferation, migration, and apoptosis of GC cells. (A) CCK-8 assays revealed that CSN3 overexpression significantly promoted GC cell proliferation. (B) Apoptosis assays by flow cytometry indicated that CSN3 overexpression decreased the apoptosis rate of GC cells. (C) Transwell assays revealed that CSN3 overexpression significantly promoted migration of GC cells. *, P<0.05; **, P<0.01; ***, P<0.001. CCK-8, Cell Counting Kit-8; CSN3, casein kappa; GC, gastric cancer; PI, propidium iodide.
Supplier Page from Abcam for Anti-RIP2 antibody