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

Journal: International Journal of Oncology

Article Title: Overcoming acquired doxorubicin resistance of ovarian carcinoma cells by verapamil-mediated promotion of DNA damage-driven cytotoxicity

doi: 10.3892/ijo.2026.5861

Figure Lengend Snippet: Cell cycle progression and proliferation following treatment of A2780 and A2780ADR cells with Topo II inhibitors. Logarithmically growing cells were treated with the indicated concentrations of Doxo or etoposide Eto for (A) 24 or (B) 72 h. Afterwards, cell cycle distribution was analyzed by flow cytometry and the percentage of cells present in different phases of the cell cycle (SubG 1 -, G1-, S- and G 2 /M-phase) was quantified. Data shown in the histogram (left panel) are the mean ± SD from n=3 independent experiments each performed in biological triplicates. The table on the right panel summarizes the mean values and indicates statistical differences between the individual groups. * P≤0.05; ** P≤0.01 (A2780 vs. A2780ADR); # P≤0.05; ## P≤0.01 (Con vs. treated group). (C) Logarithmically growing parental A2780 and Doxo resistant A2780ADR cells were treated with the indicated concentrations of Doxo (0.1 and 1.0 μ M) or Eto (1.0 and 10 μ M). At 24 h later the percentage of Ki-67 positive or pH3 positive cells was determined as described in methods. Total magnification, ×400. Quantitative data shown in the histogram are the mean ± SD from n=3 independent experiments, each performed with n=5 biological replicates. * P≤0.05; ** P≤0.01; **** P≤0.0001 (A2780 vs. A2780ADR). Con vs. treatment: # P≤0.05; ## P≤0.01; ### P≤0.001. (D) Logarithmically growing parental A2780 and Doxo resistant A2780ADR cells were treated with the indicated concentrations of Doxo (0.1 and 1.0 μ M) or Eto (1.0 and 10 μ M). At 24 h later cells were pulse-labeled with EdU for 2 h as described in Methods and the percentage of EdU positive cells was determined microscopically (total magnification, ×400). Quantitative data shown in the histogram are the mean ± SD from five biological replicates. A2780 as compared with A2780ADR: ** P≤0.05; **** P≤0.0001. Con vs. treatment: ## P≤0.01; ### P≤0.001. Doxo, doxorubicin; Eto, etoposide; SD, standard deviation.

Article Snippet: The following primary antibodies were used: Copper transporting ATPase (ATP7A), extracellular regulated kinase 2 (ERK2), phosphorylated (p)-histone H3 (Ser10) from Thermo Fisher Scientific Inc., cleaved caspase-7 (Asp198), p-Chk1 (Ser 345), cyclin B1, galactosidase β (E2U2I), GAPDH (14C10), MDR1/ABCB1 (D3H1Q), p-P53 (S15), PARP, TopBP1(D8G4L), topoisomerase IIa (D10G9), 53BP1 and Ki67 were from Cell Signaling Technology Inc., pChk2 (T68) [Y171], copper uptake protein 1 (CTR1/SLC31A1) [EPR7936] and Rad51 from Abcam, γH2AX (Ser 139) clone JBW301, p-KAP-1 (S824) and p-RPA32 (S4/S8) from Bethyl Laboratories Inc., organic cation transporter-2 (OCT2) from Biozol Diagnostics Vertrieb GmbH, p16 (F-12) and p21 (C-19) from Santa Cruz Biotechnology, Inc. As secondary antibodies, horseradish peroxidase-conjugated secondary antibodies goat anti-mouse IgG and mouse anti-rabbit IgG were used (Rockland Immunochemicals Inc.).

Techniques: Flow Cytometry, Labeling, Standard Deviation