Journal: Cancer Biology & Therapy

Article Title: UBE2S promotes gastric cancer progression through RACGAP1 stabilization associated with K292-dependent K63-linked ubiquitination

doi: 10.1080/15384047.2026.2737476

Figure Lengend Snippet: RACGAP1 restoration effectively rescues the malignant phenotypes suppressed by UBE2S knockdown. (A–B) Assessment of cell viability and clonogenic capacity in GC cells (AGS and HGC-27) transfected with shCtrl, shUBE2S, or shUBE2S + oe-RACGAP1, as determined by CCK-8 assays (A) and colony formation assays (B) ( n = 3 per group). (C–D) Evaluation of cellular motility capacity through wound-healing assays (C) and Transwell migration assays (D) across the indicated transfection groups ( n = 3 per group). (E) Western blot analysis of UBE2S, RACGAP1, total JNK, p -JNK, total c-Jun, and p -c-Jun in the indicated AGS groups with or without SP600125-mediated pharmacological JNK inhibition. (F) Representative images and quantification of colony formation under the same conditions ( n = 3 per group). (G–I) In vivo validation of the functional rescue effect using an HGC-27 xenograft model ( n = 5 per group). The analysis includes subcutaneous tumor growth kinetics (G), representative macroscopic photographs of harvested tumors (H), and statistical quantification of tumor weights (I) at the experimental endpoint (Day 35). Longitudinal tumor-volume data in (G) were analyzed using two-way repeated-measures ANOVA with Greenhouse–Geisser correction and Bonferroni-adjusted prespecified pairwise comparisons (shCtrl vs shUBE2S and shUBE2S vs shUBE2S + oeRACGAP1). Quantitative in vitro data and terminal tumor weights were analyzed by one-way ANOVA followed by LSD or Tamhane’s T2 post-hoc test, as appropriate. Data are presented as the mean ± SD. Exact pairwise comparisons are indicated in the corresponding panels.

Article Snippet: SP600125 (10 μM; TargetMol, Cat No. T3109) was used to inhibit JNK signaling.

Techniques: Knockdown, Transfection, CCK-8 Assay, Colony Assay, Migration, Western Blot, Analysis, Inhibition, In Vivo, Biomarker Discovery, Functional Assay, Xenograft Assay, In Vitro