Research Paper Volume 16, Issue 16 pp 12029—12049

Figure 9. Effects of UBR1 knockdown on proliferation, colony formation, invasion, migration, apoptosis, and NF-κB P65 pathway in AGS and MGC803 cells. (A, B) Cell Counting Kit-8 (CCK8) assay results show that cell proliferation is significantly inhibited in AGS and MGC803 cells at 24, 48, and 72 hours post-UBR1 knockdown (p < 0.001). (C) Colony formation assay indicates a significant reduction in colony formation ability in both cell lines following UBR1 knockdown. (D–F) Transwell invasion assays demonstrate a significant decrease in the invasive capacity of AGS and MGC803 cells with UBR1 knockdown (p < 0.001). (G–I) Wound healing assays reveal a significant reduction in the migratory ability of UBR1-knockdown cells (p < 0.001). (J, K) Apoptosis analysis shows an increase in apoptosis in AGS cells post-UBR1 knockdown (p < 0.01). (L–N) Western blot analysis of apoptosis-related proteins Caspase-3 and Cleaved Caspase-3 indicates an increase in Cleaved Caspase-3 expression in both cell lines after UBR1 knockdown. (O–Q) Western blot analysis of NF-κB pathway proteins shows a significant reduction in phosphorylated NF-κB P65 expression in UBR1-knockdown cells, suggesting involvement in the NF-κB pathway. In all panels, data are presented as mean ± standard deviation (SD), and statistical significance is indicated with asterisks (^*p < 0.05, ^**p < 0.01, ^***p < 0.001).