CSN3 promotes gastric cancer invasion and is associated with immune infiltration via activating NOD/TLR pathways
We found that CSN3 is highly expressed in gastric cancer and is associated with advanced tumor stage, lymph node metastasis, and poor prognosis. Functional assays showed that CSN3 promotes proliferation and migration while inhibiting apoptosis in GC cells. RNA-sequencing revealed that CSN3 overexpression predominantly activates innate immune–related pathways, particularly the NOD-like receptor and Toll-like receptor signaling pathways, suggesting a role for CSN3 in inflammatory and immune remodeling of the tumor microenvironment. Consistently, CSN3 expression was positively correlated with B-cell and CD8? T-cell infiltration, indicating that CSN3-driven transcriptional programs may link tumor aggressiveness with immune microenvironment alterations. Overall design: The study includes two groups: the experimental group (BGC823 gastric cancer cells with stable CSN3 knockdown via siRNA) and the control group (BGC823 cells transfected with empty vector). E Cells are cultured under standard conditions (37°C, 5% CO2) to the logarithmic growth phase. CSN3 knockdown efficiency is validated using qRT-PCR and Western blot, ensuring a significant reduction in expression (>70%). Total RNA is extracted using TRIzol or commercial kits, followed by DNase treatment to eliminate genomic DNA contamination.