Fig 2: Comparative expression of stem cell and CSC markers between HepG2 and HepG2_Rego_R cells. (A) Relative RNA expression levels of ABCG2, SOX2, GATA6, and CD44 using reverse transcription-quantitative polymerase chain reaction. The RNA level in HepG2 cells was regarded as 1.0 and the relative RNA expression in HepG2_Rego_R cells was calculated. (B) Protein expression levels of CD44, SOX2, ABCG2, and GATA6 were compared between the HepG2 and HepG2_Rego_R cells, and Hep3B and Hep3B_Rego_R cells using Western blotting. The relative protein expression levels were calculated based on the protein levels in HepG2 and HepG3 cells. (C) RNA expression levels of FOXM1, AURKA, and BIRC5 were compared between HepG2 and HepG2_Rego_R cells. (D) Comparative protein expression levels of FOXM1, AURKA, and BIRC5 between HepG2 and HepG2_Rego_R cells. The relative protein expression levels were calculated based on the protein levels in HepG2 cells. Statistical analysis was performed as described in Materials and Methods. Data are presented as mean ± SEM (n = 5) and were analyzed using two-way ANOVA and Bonferroni posttests (* p < 0.05, ** p < 0.01, and *** p < 0.001).

Fig 3: Increased FOXM1 expression was correlated with poor prognosis in patients with HCC and higher tumor growth in mice xenotransplantation experiments. (A–C) Kaplan–Meier survival curves were estimated using the expression levels of FOXM1, AURKA, BIRC5, CD44, SOX2, ABCG2, and VIMENTIN in The Cancer Genome Atlas database for the whole cohort of patients with HCC (n = 364) and those with hepatitis virus infection as well as HCC (n = 150).

Fig 4: Inhibition of AURKA significantly reduces the disease burden in the MPLW515L mouse model of myelofibrosisMPLW515L recipient mice were treated with 15mg/kg MLN8237 (MLN) or 60mg/kg diMF (diMF) for 3 weeks. (a,b) White cell (a) and platelet (b) counts following three weeks of treatment. MLN8237 vs vehicle and diMF vs vehicle, p ≤ 0.01 by two-way ANOVA. (c) Spleen weight of MLN8237, diMF and vehicle treated animals. (d) Percent of GFP+ cells and the degree of GFP intensity in the spleens of MPLW515L mice following treatment with MLN8237, diMF or vehicle. (e,f) The percentage of CD41+ (e), and CD42+ (f), cells in the bone marrow of treated animals. (g) DNA content of megakaryocytes stained with CD41 and DAPI. (h) TGF-β levels in the plasma of MLN8237, diMF and vehicle treated mice. (i,j) H&E (i) and reticulin (j) stained sections of bone marrow from MLN8237, diMF and vehicle treated animals. Scale bars depict 50 microns. Results are representative of 2 independent experiments. n=6 animals per group. Bar graphs and line graphs depict mean ± SD. *p ≤ 0.05, **p ≤ 0.01, compared to vehicle determined by the unpaired two-sided Student’s t test.

Fig 5: BRCA2 wild-type allele loss and Aurora A nuclear expression in breast tumours in relation to prognosis of BRCA2 999del5 mutation carriers. (A) Kaplan-Meier estimates of breast cancer-specific survival according to BRCA2 wild-type allele loss in tumours from 52 BRCA2 mutation carriers. (B) Kaplan-Meier estimates of breast cancer-specific survival according to the combination of BRCA2 wild-type allele loss and Aurora A nuclear staining in tumours from the same subgroup of 52 BRCA2 mutation carriers. All statistical tests were two sided.