Fig 2: Cell division cycle associated 2 (CDCA2) foundations via p53. (A, B). The mRNA and protein levels of the proliferation- and apoptosis-related genes in Huh7 treated with CDCA2 Si-1/2. (C, D) The proliferation of CDCA2 Si-1/2-treated Huh7 cells and LV-CDCA2-treated L02 cells at different time points detected by Cell Counting Kit-8 (CCK8) assay. (E, F) The mRNA and protein levels of the proliferation- and apoptosis-related genes in L02 treated with LV-CDCA2. *p < 0.05.

Fig 3: The expression of CDCA2 is upregulated in ESCC tissues. (A) Heatmap of the gene expression profiles of ESCC tissues and normal tissues basing on the data downloaded from TCGA. (B) Volcano map of the ESCC-related data extracted from TCGA. (C) The expression of CDCA2 in ESCC samples was significantly upregulated. ****P<0.0001. CDCA2, cell division cycle-associated 2; ESCC, oesophageal squamous cell carcinoma; TCGA, The Cancer Genome Atlas; FC, fold change; FDR, false discovery rate.

Fig 4: Identification of cell division cycle associated 2 (CDCA2). (A, B) Least absolute shrinkage and selection operator (LASSO) Cox regression analysis was performed with the expression profiles of 96 genes and survival information in The Cancer Genome Atlas (TCGA) cases, and six major prognosis-related genes were obtained. (C) The area under the curve (AUC), 95% CI, and p-values for the above six genes as diagnostic markers of hepatocellular carcinoma (HCC) were calculated in the combined Genotype-Tissue Expression (GTEx) and TCGA data. (D) Receiver operating characteristic (ROC) curve analysis was used to assess the sensitivity and specificity of CDCA2 as the marker gene of HCC. (E) Sensitivity and specificity regarding the diagnostic efficacy of CDCA2 for HCC in each fold data from the 5-fold cross-validation. (F) Confusion matrix showed that the model constructed with CDCA2 successfully predicted 228 healthy cases and 323 HCC cases.

Fig 5: CDCA2 knockdown inhibits cell viability and proliferation of 786-O and CAKI-1 cells. The expression level of CDCA2 was detected via reverse transcription-quantitative PCR to confirm the knockdown efficiency of two siRNAs in (A) 786-O and (B) CAKI-1 cells. The MTT assay demonstrated that CDCA2 knockdown inhibited the viability of (C) 786-0 and (D) CAKI-1 cells. CDCA2 knockdown significantly decreased the number of (E) 786-O and (F) CAKI-1 cell colonies compared with the control group. *P<0.05; **P<0.01; ***P<0.001; ****P<0.0001 vs. control. CDCA2, cell division cycle-associated protein 2; si, small interfering; NC, negative control.