CDC25C Antibody - #AF6258

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

(D) Effects of BCL2L10 on protein expression of PCNA and CDC25C by Western blot.

Fig. 2. The elevated TGR5 expression promotes the proliferation of the CC cell line. (A) The Western blot analysis indicated that TGR5 expession was successfully regulated with the TGR5 recombinant plasmid and siRNA targeting TGR5 in RBE cells and QBC-939 cells. The upregulation of TGR5 induced elevated expression of proliferating cell nuclear antigen (PCNA), which is involved in DNA replication-linked processes, and is a known molecular marker of proliferation, whereas silencing of TGR5 lead to a reduced expression of PCNA. Glyceraldehyde phosphate dehydrogenase (GAPDH) was used as a normalizing control. (B) CC cells treated with TGR5 siRNA revealed a weaker cell viability while these treated with TGR5 recombinant plasmid exhibited an increased cell viability, as have shown by CCK-8 assay, and this was most pronouncing at 72 h point. (C) The BrdU incorporation test revealed that the DNA synthesis in CC cells was accelerated with the TGR5 recombinant plasmid and was repressed with siRNA targeting TGR5.(D) CDC25C and cyclin D1 play a crucial role in accelerating cell cycle procession. The exposure to the TGR5 plasmid led to the augmented expression of CDC25C in RBE and QBC-939 cells, and increase the expression of cyclin D1 in QBC-939 cells. *P < 0.05 and **P < 0.01, when compared with the control group. Glyceraldehyde phosphate dehydrogenase (GAPDH) was used as a normalizing control.