Cyclin B1 Antibody - #AF6168

Figure 2 | Effect of SAD on cell cycle and apoptosis. (A) The cell cycle analysis was determined by PI staining and flow cytometry cell quest software. S1 and S1-MI-80 cells were treated with 4 μmol/L SAD for 12, 24, 48, and 72 h, respectively. The content of G2/M phase was increased in a time-dependent pattern. (B) Histograms of cell cycle distribution in non-treated and treated S1 and S1-MI-80 cells. (C) S1 and S1-MI-80 cells were treated with SAD (4 μmol/L) for four different time points. Western blot analysis was used to detect the levels of CDC2, p-CDC2 and cyclin B1 protein after SAD treatment.

Fig. 7| 4-MU inhibits glioma growth in vivo and, when combined with autophagy inhibitors, exerts synergistic effects on glioma cell viability, autophagy levels, and the cell cycle. Relative levels of the CCNB1 and CCND1 proteins in U251 glioma cells cultured with 4-MU, followed by treatment with CQ (30 μmol/L) for 48 h.

FIGURE 3 | SB induces G2/M cell cycle arrest in cervical cancer cells. (A) A marked dose-dependent increase of the percentage of cervical cancer cells in the G2/M phase arrest by flow cytometry. (B) The protein expression levels of CDK1, cyclin B1, and cdc25C at 24 h after SB treatment. Expression levels were normalized to the β-actin protein level. Values (mean ± SDs) were obtained from at least three independent experiments. *P < 0.05, **P < 0.01, and ***P < 0.001 by one-way ANOVA with Tukey’s test

Figure 6 KIF11, KIF11-CDK1-CDC25C-cyclinB1 oncogenic network and NF-kB/JNK signaling pathway are the potential CVB-D therapeutic targets in the NSCLC cells. (A) Venn diagram showed the overlap number of potential CVB-D target genes in NSCLC cells by intersecting four LUAD datasets. (B) Protein-protein interaction network analysis revealed interaction between the 10 overlapping DEGs. The disconnected nodes are hidden. (C) The interactive heatmap from GEPIA 2 database showed expression of the 6 DEGs in LUAD and normal lung tissues. KIF11 is the most differentially expressed gene between LUAD and normal lung tissues. (D) Venn diagram revealed 2 common genes (KIF11 and CDK1) based on intersection between the 10 overlapping DEGs and the 100 predicted CVB-D target genes extracted from the Swisstarget prediction database. (E) Western blot analysis identified the expression of KIF11, CDK1, CDC25C and cyclinB1 proteins in the control and CVB-D-treated NSCLC cells. (F and G) Immunohistochemical assay results showed the expression levels and localization of the KIF11 protein in the control and CVB-D-treated A549 xenograft tumor tissues. (H) Western blot assay results revealed the KIF11 protein levels in the si-NC and si-KIF11-transfected NSCLC cells. (I) Western blot analysis demonstrated the expression levels of the oncogenic signaling network proteins (KIF11, CDK1, CDC25C and CyclinB1) and the NF-κB/JNK signaling pathway proteins (p65, p-p65, JNK and p-JNK) in the si-NC- and si-KIF11-transfected NSCLC cells. **P

Figure 7 CVB-D inhibits in vivo progression of A549 xenografts tumors. (A) Experimental design for tumor xenograft experiments of NSCLC in nude mice to evaluate the in vivo therapeutic effects of CVB-D. Specific time points for CVB-D treatment and experimental analysis are indicated. (B) Representative images of the NSCLC xenograft tumor models with or without CVB-D treatment. (C) Representative images of the NSCLC xenograft tumor tissues from control and CVB-D-treated mice. (D and E) NSCLC xenograft tumor weights and volumes in the control and CVB-D treatment groups of nude mice. (F) Representative H&E and TUNEL staining images of the A549 xenograft tumor sections in the control and CVB-D treatment groups of nude mice (magnification, ×200; scale bar, 50 µm). (G) The proportion of apoptotic cells in the A549 xenograft tumors derived from the control and CVB-D-treatment groups of nude mice based on TUNEL staining. (H) The body weights of the xenograft tumor model mice in the control and CVB-D treatment groups. (I and J) Immunohistochemical assay data revealed the expression levels and distribution of CDK1, CDC25C, cyclinB1, Ki67, Bcl-2 and N-cadherin proteins in the A549 xenograft tumors derived from the control and CVB-D treatment groups (magnification, ×200; scale bar, 50 µm). *P

Fig 5. |Western blot results. (a) The levels of cyclin A, cyclin B, cyclin D1, and CDK2 were reduced in A375 cells transfected with OVOS2-shRNA

Figure 3.| Naringenin arrests cell cycle progression of renal cell carcinoma cells in the G2 phase. 786‑O and OS‑RC‑2 cells were treated with naringenin (0, 4 or 8 µM) for 48 h. (A) Cell cycle distribution was determined using flow cytometry. (B) Western blot analysis of cyclin E1, cyclin A2, cyclin B1, cyclin D1, P27 and P21 expression levels. Data are presented as the mean ± SD. * P<0.05, **P<0.01 vs. Abs. Abs, absolute ethanol.