Fig 1: Induction of CDK-cyclin pathway activation by KU + Y at the early and late stages after treatment.a, b and d Representative immunoblots of the indicated cell cycle regulators at 1 DPT (a), 3 DPT (b) or 8 DPT (d) with KU, Y, or KU + Y. The arrows indicate the bands representing the phosphorylated forms of the proteins. c and e The protein levels of cyclins (c), P21, and P16 (e bottom) and the levels of phosphorylated RB and P53 (e top) were quantified using images acquired from N = 2–4 samples per experiment. The data are shown as the mean ± s.d. values. *P < 0.05; **P < 0.01; ***P < 1.0 × 10-3; ****P < 1.0 × 10-4 by one-way ANOVA with Tukey’s post hoc correction.
Fig 2: Knockdown of p16 decreases IL6 and CXCL8 expression in oncogene-induced senescent cells. IMR90s expressing either BRAFV600E or HRASG12V alone or in combination with a shRNA targeting p16 (shp16 hairpin #1). An empty pBabe retroviral vector and a shRNA targeting GFP lentiviral vector were used as controls. See Supplementary Figure 1A for an experimental timeline. (A) Immunoblot of BRAF and p16. Vinculin was used a loading control. (B) Representative images of senescence-associated ß-galactosidase (ß-GAL) staining and colony formation (CF). (C) Quantification of ß-GAL in (B). (D) Quantification of CF in (B). (E) Immunoblot of RAS and p16. ß-actin was used as loading control. (F) Representative images of ß-GAL staining and colony formation (CF). (G) Quantification of ß-GAL in (F). (H) Quantification of CF in (F). (I, J) IL6 and CXCL8 mRNA expression (fold change relative to control mean). Expression of target genes was normalized against multiple reference genes. Data normalized against MRPL9 are shown. n=3/group and mean±SD. 1 out of 3 experiments is shown. *p<0.05.
Fig 3: Irisin inhibits nicotine-mediated endothelial cell senescence and cell cycle arrest. (A) ß-Gal staining of HUVECs after phase I and II interventions. (B) Quantification of the ß-gal positive staining percentage. (C) Immunoblotting bands of P53, P21, P16, and GAPDH after phase I and II interventions. (D) Quantification of western blot of P53, P21, and P16. (E) Propidium iodide (PI) cell cycle assay performed at 12 and 24 h during phase II intervention. (F) G0/G1, S, and G2/M phase proportions at 12 and 24 h during phase II intervention. (G) Quantitative RT-PCR of CDK1. All results were normalized to the expression level of GAPDH and presented as the fold change of the Control group. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001. Data are mean ± SD; ns, no significance, n = 3.
Fig 4: Associations between INK4 family members and immune cell infiltration in HCC(A) The correlation analysis of CDKN2A and the infiltration levels of six types of immune cells (macrophages, neutrophils, dendritic cells, CD4+ T cells, CD8+ T cells, and B cells). (B) The correlation analysis of CDKN2B and the infiltration levels of immune cells. (C) The correlation analysis of CDKN2C and the infiltration levels of immune cells. (D) The correlation analysis of CDKN2D and the infiltration levels of immune cells.
Fig 5: CDKN2A disruption cooperates with IL7Rins for full leukemic transformation CD34 + human cord blood (CB) progenitors.a Flow cytometer scatter plot of human-engrafted cells in BM of untransduced CB and leukemic mice. b Sanger sequencing electropherogram of gDNA from CD45+ cells of leukemic mice surrounding guide 2 targeting CDKN2A, demonstrating disruption of the locus in leukemic cells. c Scheme of leukemia development after aberrant activation of IL7RA.
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