The prevalence of type-specific HPV infection in women with normal cytology in the HK and GZ cohorts.

<p>*Statistically significant at 0.05 level of significance by Holm's procedure that accounts for the multiple comparisons.</p><p>**Adjusted for the stratified sampling design.</p>†<p>The seven commonest HPV high-risk types in the HK cohort.</p>‡<p>The seven commonest HPV high-risk types in the GZ cohort.</p

Potential risk factors in relation to HPV infection in the HK and GZ cohorts.

1<p>:Tolerance >0.4 for all variables, Naglekerke R² = 7.8%, Hosmer-Lemeshow test p = 0.793.</p>2<p>:Tolerance >0.4 for all variables, Naglekerke R² = 3.5%, Hosmer-Lemeshow test p = 0.750.</p>3<p>:OR and P-value were obtained using multivariate logistic regression analysis model of which included all of the variables listed in this table. Bold type indicated statistically significant values.</p><p>N: Total number of cases.</p

Comparison of the age-specific overall and high-risk HPV prevalence in five age-groups in the HK and GZ cohorts.

<p>(A) Overall HPV prevalence: significant difference in the overall HPV prevalence between the two cohorts in age-groups of 30–39, 40–49 and 50–59 (p<0.001, p<0.001 and p = 0.007, respectively, z test). (B) High-risk HPV prevalence: significant difference in the high-risk HPV prevalence between the two cohorts in age-groups of 30–39 and 40–49 (p<0.001 and p<0.001, respectively, z test). The error bar indicates 95% confidence interval.</p

Paclitaxel treatment down-regulates FOXM1 expression in SKOV-3 but not in SKOV3-TR cells.

<p>The paclitaxel sensitive SKOV-3 and resistant SKOV3-TR ovarian cancer cells were treated with 100 nM paclitaxel and harvested at times indicated for Western blot analysis. Paclitaxel treatment down-regulated FOXM1 expression at time points 48 h and 72 h in SKOV-3 but not in SKOV3-TR as shown by immunoblotting. There were also no marked changes in the cleaved Caspase-9 and Caspase-7 expression.</p

Transient FOXM1 knockdown significantly enhanced paclitaxel-induced mitotic catastrophe in SKOV-3 and OVCAR3 cells.

<p>SKOV-3 and OVCAR3 cells transfected with either siRNA pools against FOXM1 or control siRNA pools were treated with paclitaxel (100 nM) and stained with DAPI. <b>A.</b> Representative staining results were shown showing that transient FOXM1 knockdown significantly enhanced paclitaxel-induced mitotic catastrophe (arrow) in SKOV-3 and OVCAR3 cells respectively (Upper panel). <b>B</b>. Graphs represent the results of three independent experiments, showing the percentage of cells undergoing mitotic catastrophe, * P<0.05, significant; Mann-Whitney <i>U</i>-test.</p

Flow cytometric analysis of SKOV-3 and SKOV-3-TR cells with and without FOXM1 depletion in the presence or absence of paclitacel treatment.

<p><b>A</b>. Flow cytometric analysis was performed following propidium iodide staining on SKOV-3 and SKOV-3-TR cells treated with paclitaxel (100 nM) or remained untreated after transfection with siRNA pools against FOXM1 or control siRNA pools. Representative data are shown indicating that FOXM1 silencing is capable of increasing the number of dead cells and cells blocked at G2/M cell cycle phase in SKOV-3-TR as compared to cells treated with control siRNA. <b>B</b>. Bar charts of different phases of cell cycle in SKOV-3 and SKOV3-TR treated with paclitaxel after transfection with control or siRNA against FOXM1. Results represent data from two independent experiments.</p

Summary of nuclear FOXM1 immunohistochemical staining results in various types of ovarian tumors.

<p>*p value reflects the comparison of serous ovarian cancer vs. all the other histological types combined.</p>†<p>p value reflects the comparison of stage I vs. stage II–IV.</p>‡<p>p value reflects the comparison of low grade (grade I) vs. high grade (grade II and III).</p>Υ<p>p value reflects the comparison of chemosensitive vs chemoresistant cases.</p><p>Summary of nuclear FOXM1 immunohistochemical staining results in various types of ovarian tumors.</p

Identification of KIF2C as a novel FOXM1 transcriptional target that might be implicated in the acquisition of paclitaxel resistance.

<p><b>A</b>, Paclitaxel treatment (50 nM) down-regulated FOXM1 and KIF2C expressions at 48 h and 72 h in PEO1 but not in PEO1-TaxR. <b>B</b>, FOXM1 knockdown significantly reduced the transcript level of KIF2C in PEO1 and PEO1-TaxR. Data represent triplicates from three experiments. *P = 0.04, ***P = 0.0003. siControl: Non-specific control. siFOXM1: FOXM1 knockdown. <b>C</b>, ChIP-qPCR showed FOXM1 significantly pull down KIF2C promoter region in PEO1 and PEO1-TaxR as compared to the negative IgG control. Data represent triplicates from three experiments. *P = 0.04, ***P = 0.0001. <b>D</b>, Schematic diagram depicting locations of forkhead response element (FHRE) and the binding site of primers used in ChIP-qPCR upstream of the transcription start site of KIF2C.</p

Composition of buffers used in ChIP.

<p>Composition of buffers used in ChIP.</p

Silencing of FOXM1 reduced migration and invasion of SKOV-3.

<p><b>A</b>. Representative images showing cells migrated (gelatin-coated membrane) or invaded (matrigel-coated membrane) after 24 h. <b>B</b>. Representative Western blot analysis demonstrating the effectiveness of FOXM1 transient knockdown in SKOV-3. <b>C</b>. Graphic representation of migration (left panel) and invasion (right panel) results as fold change of migrated and invaded cells relative to the control, respectively, in five fields of triplicate wells from three independent experiments; * P<0.05, significant; Mann-Whitney <i>U</i>-test.</p