Research Paper Volume 13, Issue 16 pp 20094—20115

Overexpressed DEPDC1B contributes to the progression of hepatocellular carcinoma by CDK1


Figure 5. Obtained the DEGs by human GeneChip PrimeView and the expression at mRNA and protein level. (A) Genes were represented as red points or green points, when Fold Change ≤-1.5 and FDR<0.05 or Fold Change ≥1.5 and FDR<0.05. (B) Up-regulated genes and down-regulated genes were labeled as red and green, respectively. (C) Salvage Pathways of Pyrimidine Ribonucleotides, NER Pathway, Estrogen-mediated S-phase Entry, and Cyclins and Cell Cycle Regulation were significantly inhibited. (D) The enrichment of DEGS in disease and function. (E) The interaction network between DEPDC1B, Cyclins and Cell Cycle Regulation, and Wnt/β-catenin Signaling pathway. (F) The results of qRT-PCR showed that, compared to shCtrl group, the expression level of E2F1, CCNA1, TFDP1, CCNA2, FOS, UBA52, CCNB1, JUN, CCNB2, CCNE2, MYC, CDK1, CDK2, CDK6, RBL1, CDKN2C, CDC25A, SKP2, DKK1, and TCF3 was down-regulated (P<0.05). (G) The results of western blot showed that CCNE2, CDK1, CDK6, and E2F1was significantly down-regulated in shDEPDC1B group, compared to shCtrl group. (H) The results of IHC showed that the expression level of CDK1 in cancer tissues was higher than in normal tissues (scale bar = 50 μm).