Prevalence and Risk Factors of Human Papillomavirus (HPV) Infection in Southern Chinese Women – A Population-Based Study

Background: Persistent high-risk type Human papillomavirus (HPV) infection is recognized as a necessary cause of cervical cancer. This study aimed to compare the HPV prevalence and risk factors between women residing in Hong Kong (HK) and Guangzhou (GZ) region of China. Methodology/Principal Findings: A total of 1,570 and 1,369 women were recruited from HK and GZ, respectively. The cytology samples were collected and tested for HPV infection. The overall and type-specific HPV prevalence and the potential risk factors for acquisition of HPV infection were studied. Women with normal cytology in the GZ cohort had significantly higher HPV prevalence (10%) than those in the HK cohort (6.2%, p<0.001). The patterns of the age-specific HPV prevalence were also different between the two cohorts. In the HK cohort, women at the age of 20-29 years old had the highest prevalence and a second peak was observed in the age of ≥60 years old. In the GZ cohort, the highest HPV prevalence was also observed in 20-29 years old but declined as the age increased and a second peak was not seen. HPV16 and HPV52 were the most common high-risk types found in the HK and GZ cohorts, respectively. Age was the most consistently observed independent risk factor for HPV infection in the HK, while the number of sexual partners had association in the GZ cohort. Conclusions/Significance: Our study provides the current status and the epidemiological characteristics of HPV prevalence in Southern Chinese women. The results strongly suggested that population education and the effective cervical cancer screening would be vital in the prevention of cervical cancer. © 2011 Liu et al.published_or_final_versio

The clinical significance of serum squamous cell carcinoma antigen (SCC) in carcinoma of cervix

published_or_final_versionMedicineMasterDoctor of Medicin

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GADD45α contributed to TAp73-mediated apoptosis in response to cisplatin.

<p>Cell apoptosis was diminished in TAp73α-overexpressed cells (SKOV3 C8 and OVCA433 C1) in response to cisplatin after GADD45α siRNAs treatment. The cell apoptosis was measured by (A) TUNEL assay (error bars indicate mean ± SD from three independent experiments; *: p<0.05; **: p<0.01) and (B) the cleavage of PARP assay.</p

A proposed model for the regulatory role of TAp73 in DNA damage response.

<p>DNA damage agent, cisplatin induces TAp73 accumulation and the subsequent up-regulation of its pro-apoptotic target genes to induce cell apoptosis. Simultaneously, up-regulation of TAp73 target gene, GADD45α activates the JNK apoptotic pathway via its interaction with MEKK4/MTK1 to induce apoptosis.</p

Overexpression of TAp73α promoted cell apoptosis in response to cisplatin.

<p>(A) TAp73α-overexpressed cells (SKOV3 C8, C24 and C28 and OVCA433 C1, C7 and C12) and the empty vector controls (V) of SKOV3 and OVCA433 were treated with 4 μg/ml cisplatin for 48 h. Apoptotic cells were assessed by TUNEL assay. More than 500 cells were counted for each group, the results presented were the relative of the apoptotic cells to total cells and at least three independent experiments were performed (**: p<0.01). (B) TAp73α-overexpressed cells and empty vector controls were treated with different doses (indicated) of cisplatin for 24 h, and the cleavage of PARP was detected by western blot analysis.</p

TAp73α activated the JNK pathway through up-regulating GADD45α and the subsequent activation of MKK4.

<p>(A) Increase of GADD45α mRNA expression in TAp73α-overexpressed cells (SKOV3 C8, C24 and C28 and OVCA433 C1, C7 and C12). (B) Increase of GADD45α protein expression and the MKK4 phosphorylation level in TAp73α-overexpressed cells (SKOV3 C8, C24 and C28 and OVCA433 C1, C7 and C12). (C) GADD45α was knocked down in TAp73α-overexpressed cells (SKOV3 C8 and OVCA433 C1) by siRNAs (Si1-GADD45α and Si2-GADD45α) treatment. The activation of MKK4, JNK and c-Jun were diminished, even under the cisplatin treatment.</p

Activation of JNK was involved in TAp73α-mediated apoptosis induced by cisplatin.

<p>(A) TAp73α-overexpressed cells (SKOV3 C8 and OVCA433 C1) were treated with 20 μM SP600125 for different periods of time (indicated). The phosphorylation levels of JNK and c-Jun were measured. (B and C) TAp73α-overexpressed cells (SKOV3 C8 and OVCA433 C1) and the empty vector controls (V) were treated with 20 μM SP600125 or DMSO and then with cisplatin. The cell apoptosis were assessed by TUNEL assay (error bars indicated mean ± SD from three independent experiments; *: p<0.05) and the cleavage of PARP analysis. Inhibition of JNK attenuated TAp73α-mediated apoptosis in response to cisplatin. (D) TAp73α-overexpressed cells (SKOV3 C8 and OVCA433 C1) were treated with JNK siRNAs (Si-JNK) or the scrambled control siRNA (Control). The activations of JNK and c-Jun were absent upon cisplatin treatment, and associated with markedly reduced cell apoptosis (E and F).</p

Overexpression of TAp73α enhanced cellular sensitivity to cisplatin.

<p>(A) The GFP-TAp73α overexpressing stable clones in SKOV3 (C8, C24 and C28) and OVCA433 (C1, C7 and C12) cells were verified by western blot analysis. (B and C) Both XTT viability assay and clonogenic assay showed significantly reduced cell proliferation in TAp73α-overexpressed cells of SKOV3 and OVCA433 compared to the empty vector controls (V) in response to cisplatin treatment. The percentage of cells/colonies surviving in cisplatin relative to cells/colonies in drug-free medium control was measured. Data was shown as mean ± SD from three independent experiments (*: p<0.05; **: p<0.01).</p