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NUFIP2 mediates ESCO1-driven tumor growth, and ESCO1 interacts with NUFIP2 to maintain its protein stability. (A) Xenograft tumor growth following ESCO1 knockdown, NUFIP2 knockdown, or NUFIP2 restoration. (B) Immunohistochemical staining <t>of</t> <t>Ki-67</t> and BCL-2 in xenograft tumors. (C) Confocal immunofluorescence analysis of ESCO1 and NUFIP2 colocalization. (D, E) Co-IP analysis of the interaction between ESCO1 and NUFIP2 in PANC-1 and SW1990 cells. (F) NUFIP2 mRNA expression following ESCO1 knockdown. (G–I) CHX chase analysis of NUFIP2 protein stability in PANC-1 and SW1990 cells. **P < 0.01, ***P < 0.001,****P < 0.0001.
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In vivo therapeutic efficacy of advanced BAITs in a postoperative tumor model. (A) Schematic of in vivo experimental design. LLC tumors were surgically resected, and mice were re-challenged with LLC cells. Mice then received BAIT treatments. (B) Photographs of tumors and tumor weights at day 16 for each group (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗ is P < 0.001 by one-way ANOVA with Bonferroni post-hoc test). (C) Individual tumor growth curves over time (n = 5; ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (D) H&E-stained tumor sections. (E) TUNEL staining of tumor sections (brown, apoptotic cells). Black arrowheads mark TUNEL + areas. (F) Quantification of TUNEL + apoptotic cells (n = 5; ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). (G) Representative immunofluorescence for <t>Ki67</t> (green) in tumor tissues (nuclei in blue). The Apo-BAIT group shows greatly reduced Ki67 + proliferating cells. (H) Quantification of Ki67 + cell density (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). Data are presented as mean ± SD.
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NUFIP2 mediates ESCO1-driven tumor growth, and ESCO1 interacts with NUFIP2 to maintain its protein stability. (A) Xenograft tumor growth following ESCO1 knockdown, NUFIP2 knockdown, or NUFIP2 restoration. (B) Immunohistochemical staining of Ki-67 and BCL-2 in xenograft tumors. (C) Confocal immunofluorescence analysis of ESCO1 and NUFIP2 colocalization. (D, E) Co-IP analysis of the interaction between ESCO1 and NUFIP2 in PANC-1 and SW1990 cells. (F) NUFIP2 mRNA expression following ESCO1 knockdown. (G–I) CHX chase analysis of NUFIP2 protein stability in PANC-1 and SW1990 cells. **P < 0.01, ***P < 0.001,****P < 0.0001.

Journal: Frontiers in Immunology

Article Title: ESCO1 stabilizes NUFIP2 through acetylation–ubiquitination crosstalk to promote pancreatic cancer progression

doi: 10.3389/fimmu.2026.1929713

Figure Lengend Snippet: NUFIP2 mediates ESCO1-driven tumor growth, and ESCO1 interacts with NUFIP2 to maintain its protein stability. (A) Xenograft tumor growth following ESCO1 knockdown, NUFIP2 knockdown, or NUFIP2 restoration. (B) Immunohistochemical staining of Ki-67 and BCL-2 in xenograft tumors. (C) Confocal immunofluorescence analysis of ESCO1 and NUFIP2 colocalization. (D, E) Co-IP analysis of the interaction between ESCO1 and NUFIP2 in PANC-1 and SW1990 cells. (F) NUFIP2 mRNA expression following ESCO1 knockdown. (G–I) CHX chase analysis of NUFIP2 protein stability in PANC-1 and SW1990 cells. **P < 0.01, ***P < 0.001,****P < 0.0001.

Article Snippet: The sections were then incubated overnight at 4 °C with primary antibodies against ESCO1(1:500), NUFIP2(1:500), BCL-2 (1:500, Cat. No. 12789-1-AP, Proteintech Group, Inc., Wuhan, China), or Ki-67 (1:500, Cat. No. 27309-1-AP, Proteintech Group, Inc., Wuhan, China).

Techniques: Stability, Xenograft Assay, Knockdown, Immunohistochemical staining, Staining, Confocal, Immunofluorescence, Analysis, Co-Immunoprecipitation Assay, Expressing

In vivo therapeutic efficacy of advanced BAITs in a postoperative tumor model. (A) Schematic of in vivo experimental design. LLC tumors were surgically resected, and mice were re-challenged with LLC cells. Mice then received BAIT treatments. (B) Photographs of tumors and tumor weights at day 16 for each group (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗ is P < 0.001 by one-way ANOVA with Bonferroni post-hoc test). (C) Individual tumor growth curves over time (n = 5; ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (D) H&E-stained tumor sections. (E) TUNEL staining of tumor sections (brown, apoptotic cells). Black arrowheads mark TUNEL + areas. (F) Quantification of TUNEL + apoptotic cells (n = 5; ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). (G) Representative immunofluorescence for Ki67 (green) in tumor tissues (nuclei in blue). The Apo-BAIT group shows greatly reduced Ki67 + proliferating cells. (H) Quantification of Ki67 + cell density (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). Data are presented as mean ± SD.

Journal: Bioactive Materials

Article Title: Countering postoperative immune suppression with a self-assembling dendritic cell nanovaccine

doi: 10.1016/j.bioactmat.2026.05.005

Figure Lengend Snippet: In vivo therapeutic efficacy of advanced BAITs in a postoperative tumor model. (A) Schematic of in vivo experimental design. LLC tumors were surgically resected, and mice were re-challenged with LLC cells. Mice then received BAIT treatments. (B) Photographs of tumors and tumor weights at day 16 for each group (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗ is P < 0.001 by one-way ANOVA with Bonferroni post-hoc test). (C) Individual tumor growth curves over time (n = 5; ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (D) H&E-stained tumor sections. (E) TUNEL staining of tumor sections (brown, apoptotic cells). Black arrowheads mark TUNEL + areas. (F) Quantification of TUNEL + apoptotic cells (n = 5; ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). (G) Representative immunofluorescence for Ki67 (green) in tumor tissues (nuclei in blue). The Apo-BAIT group shows greatly reduced Ki67 + proliferating cells. (H) Quantification of Ki67 + cell density (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). Data are presented as mean ± SD.

Article Snippet: Anti-Ki67 mouse mAb (Cat# GB121141-100), anti-CD3 mouse mAb (Cat# GB15014-100), FITC-conjugated goat anti-mouse IgG (H + L) (Cat# GB22301), and Cy5-conjugated goat anti-mouse IgG (H + L) (Cat# GB27301) for immunofluorescence assays, and DAB (SA-HRP) TUNEL apoptosis detection kit were supplied by Servicebio (Wuhan, China).

Techniques: In Vivo, Drug discovery, Staining, TUNEL Assay, Immunofluorescence