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

Journal: Non-coding RNA Research

Article Title: The regulatory role of circGDI2 in hepatocellular carcinoma proliferation and glycolysis with the involvement of m6A modification

doi: 10.1016/j.ncrna.2025.11.006

Figure Lengend Snippet: Silencing circGDI2 inhibits HCC tumor growth and PKM2 expression through IGF2BP2. To verify the effect of circGDI2 and IGF2BP2 on HCC tumor growth, a xenograft mouse model was constructed. (A) Pictures of the isolated tumors of the indicated group. (B) The tumor volume and weight were recorded. (C) HE staining, Tunel and Ki-67 staining were performed to observe the histological characteristics and cell proliferation in the tumor tissues (scale bar = 100 μm). (D) RT-qPCR was used to detect circGDI2, IGF2BP2 and PKM2 levels. (E) IHC was used to detect IGF2BP2 and PKM2 levels (scale bar = 100 μm). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, vs. the sh-NC group. # P < 0.05, ## P < 0.01, ### P < 0.001, vs. the sh-circGDI2+OE-NC group.

Article Snippet: Ki67 , IHC , Rabbit , 1:500 , Proteintech , 84432-1-RR.

Techniques: Expressing, Construct, Isolation, Staining, TUNEL Assay, Quantitative RT-PCR

Journal: Non-coding RNA Research

Article Title: The regulatory role of circGDI2 in hepatocellular carcinoma proliferation and glycolysis with the involvement of m6A modification

doi: 10.1016/j.ncrna.2025.11.006

Figure Lengend Snippet: Silencing FTO inhibits HCC tumor growth and decreases circRNA, IGF2BP2 and PKM2 levels. To investigate the biological role of FTO on HCC tumor growth, the xenograft tumor models of HCC cells in the sh-NC and sh-FTO groups were established. (A) Pictures of the isolated tumors of the indicated group. (B) The tumor volume and weight were recorded. (C) HE staining, Ki-67 staining and Tunel stainning were performed to observe the histological characteristics and cell proliferation in the tumor tissues (scale bar = 100 μm). (D) RT-qPCR was used to detect circGDI2 and FTO levels. (E) IHC was used to detect IGF2BP2 and PKM2 levels (scale bar = 100 μm). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, vs. the sh-NC group.

Article Snippet: Ki67 , IHC , Rabbit , 1:500 , Proteintech , 84432-1-RR.

Techniques: Isolation, Staining, TUNEL Assay, Quantitative RT-PCR