Article Figures & Data
Figures
- Figure 1.
CRY1 and NANOG expression in normal cervical epithelial, low-grade cervical intraepithelial neoplasia (CIN), high-grade CIN, and cervical cancer tissues. (A) Representative immunohistochemical images of CRY1 and NANOG in normal cervical epithelial, low-grade CIN, high-grade CIN, and cervical cancer tissues. Scale bar: 50 μm (B) Comparison of IHC staining score for CRY1 in normal cervical epithelial, low-grade CIN, high-grade CIN, and cervical cancer tissues and between stage I and stages II-IV in cervical cancer tissues. Comparison of IHC scoring for NANOG in normal cervical epithelial, low-grade CIN, high-grade CIN, and cervical cancer tissues and between good and poor chemoradiation response in cervical cancer patients. (C) Combined over-expression of CRY1 and NANOG showed more predictive value for the response to chemoradiation treatment over single gene expression of CRY1 or NANOG.
- Figure 2.
Kaplan–Meier survival curves for CRY1 and NANOG expression in cervical cancer. Patients with cervical cancer over-expressing CRY1 showed worse (A) overall survival (p=0.001) and (D) disease-free survival (p=0.001) than those with low expression of CRY1. Cervical cancer patients with NANOG over-expression showed worse (B) overall survival (p=0.001) and (E) disease-free survival (p=0.001). Patients with over-expression of both CRY1 and NANOG showed worse (C) overall survival (p<0.001) and (F) disease-free survival (p<0.001) compared to patients with low expression of both CRY1 and NANOG.
- Figure 3.
Effect of CRY1 in cervical cancer cell lines. CRY1 was knocked down in Caski and SNU-17 cells for 72 h. (A) Protein expression of CRY1 and α-actinin was analysed by western blot. (B) The proliferation of siControl- and siCRY1-transfected Caski and SNU-17 cells was detected using EZ-Cytox assay, at indicated time points. (C) Colony formation was performed with siControl and siCRY1 transfected cell. Upper panel: representative image of colonogenic assay. Lower panel: quantitative results of colonogenic assay. (D) Cell invasion assay was conducted using the Boyden chamber assay. Upper panel: representative image of Boyden chamber assay. Lower panel: quantitative result of Boyden chamber assay. The number of asterisks (*) indicates the level of significance: **p<0.05, ***p<0.005. Error bars represent the mean±standard error (S.E) of triplicate experiments.
- Figure 4.
Effect of NANOG expression in cervical cancer cell lines. NANO. G was knocked down in Caski and SNU-17 cells for 72 (A) Protein expression of NANOG and α-actinin was analysed by western blot. (B) The proliferation of siControl- and siNANOG-transfected Caski and SNU-17 cells was detected using EZ-Cytox assay, at indicated time points. (C) Colony formation was performed with siControl and siCRY1 transfected cell. Upper panel: representative image of colonogenic assay. Lower panel: quantitative results of colonogenic assay. (D) Cell invasion assay was conducted using the Boyden chamber assay. Upper panel: representative image of Boyden chamber assay. Lower panel: quantitative result of Boyden chamber assay. The number of asterisks (*) indicates the level of significance: **p<0.05, ***p<0.005. Error bars represent the mean±standard error (S.E) of triplicate experiments.
- Figure 5.
Effects of CRY1 in apoptosis and correlation with NANOG expression in cervical cancer specimens and cell lines. (A) Spearman’s rank correlation analysis showed the positive correlation between CRY1 and NANOG expression in cervical cancer specimens (B) Caski and SNU-17 cells were treated with the indicated concentration of cisplatin for 48 h. Cells were harvested; protein expression of CRY1, PARP, Caspase-3, and α-actinin was analyzed by western blot. (C) CRY1 was knocked down in Caski and SNU-17 cells for 48 h and then cells were treated with 100 μM cisplatin for 48 h. Cells were then harvested and apoptosis was analyzed using flow cytometry after staining with annexin V-FITC/propidium iodide. Upper panel: representative scatter plots of propidium iodide (y-axis) versus annexin V (x-axis). Lower panel: Quantitative analysis of the apoptotic cells. (D) CRY1 was knocked down in Caski and SNU-17 cells for 72 h. Cells were then harvested and protein expression and activation status of CRY1, p53, P-STAT3, STAT3, NANOG, and α-actinin were analysed by western blot. The number of asterisks (*) indicates the level of significance: **p<0.05, ***p<0.005. Error bars represent mean±standard error (S.E) of triplicate experiments.
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