Fig 1: Expressions of the core genes in different breast cancer research microarrays. (A) CENPF expression in TCGA breast (1: breast, 2: invasive lobular breast carcinoma). (B) SKA1 expression in Turashvili breast (1: ductal breast cell, 2: lobular breast cell, 3: invasive ductal breast carcinoma). (C) BIRC5 expression in Curtis breast (1: breast, 2: medullary breast carcinoma). (D) CENPA expression in Curtis breast (1: breast, 2: invasive ductal breast carcinoma). (E) CCNB2 expression in Turashvili breast (1: ductal breast cell, 2: lobular breast cell, 3: invasive ductal breast carcinoma).
Fig 2: Cellular changes in HCT116 p53-/- cells after knocking down CSE1L expression. (A) Knockdown efficacy of CSE1L in HCT116 p53-/- cells. (B) Protein expression levels of CSE1L in HCT116 p53-/- cells without or with CSE1L knockdown. (C) Population of HCT116 p53-/- cells in the various phases of cell cycle without or with CSE1L knockdown. (D) Percentages of shCSE1L-HCT116 p53-/- cells in the various phases of cell cycle without or with knockdown of CSE1L expression were quantified. (E) Protein expression levels of CCNA2, CCNB2 and CCND1 in HCT116 p53-/- cells without or with CSE1L knockdown. *P<0.05, **P<0.01 and ***P<0.001. HCT116 p53-/-, p53-null HCT116 cells. shLuc, lentiviral construct targeting luciferase; shCSE1L, lentiviral construct targeting CSE1L; sh, short hairpin; CSE1L, chromosome segregation 1-like protein; CCNA2, cyclin A2; CCNB2, cyclin B2; CCND1, cyclin D1.
Fig 3: Prognostic values of mRNA expression levels of the core genes in patients with triple-negative breast cancer (Kaplan–Meier analysis). (A) Association of BIRC5 with RFS in TNBC. (B) Association of CENPA with RFS in TNBC. (C) Association of SKA1 with RFS in TNBC. (D) Association of CENPF with RFS in TNBC. (E) Association of CCNB2 with RFS in TNBC.
Fig 4: Kaplan–Meier overall survival curves according to the (A) patient age (p = 0.170), (B) tumor size (p = 0.143), and (C) CCNB2 expression (p = 0.022).
Fig 5: Snf2h regulates transcription by altering chromatin accessibility. (A) Metaplot showing the ATAC-seq signals at transcription start sites (TSSs) in WT and CKO growing oocytes (GO1) and fully grown GV oocytes (FGO). (B) Heat map showing the ATAC peaks classified according to their changes in CKO versus WT oocytes. Each row represents a locus (ATAC-seq peak center ± 5 kb), and the green gradient color indicates the ATAC-seq signal intensity. (C) Metaplot showing the ATAC-seq signals at TSS of down-regulated genes in CKO FGO. (D) Genome browser views showing the ATAC-seq and RNA-seq signals at Prkar2b, Ccnb2, and Ndc80 loci. The pink boxes indicate the ATAC peaks at the promoter regions, and the green boxes indicate the RNA-seq signals.
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