ABSTRACT.We investigated a possible association between CASP-10 gene polymorphisms and susceptibility to cancer through a meta-analysis. Eight studies with a total of 29,936 cancer cases and 34,041 healthy controls were included. Meta-analysis results showed that the rs13006529*T carrier was significantly associated with increased cancer risk (OR = 1.17, 95%CI = 1.01-1.36, P = 0.03). However, rs3900115 and rs13010627 showed no association with cancer susceptibility (all P > 0.05). In the subgroup analysis by cancer type, we found that the rs13006529*T carrier was a risk factor for breast cancer (OR = 1.17, 95%CI = 1.01-1.36, P = 0.03). Similarly, no association was found between CASP-10 polymorphisms and susceptibility to lymphoma, myeloma, melanoma, or lung cancer (all P > 0.05). This meta-analysis suggests that the rs13006529*T carrier in the CASP-10 gene might be a risk factor for cancer susceptibility, especially for breast cancer.

Background. Breast cancer remains the leading cause of cancer-related mortality worldwide. It has been indicated that human papillomaviruses 16 (HPV16) might participate in the pathogenesis and development of breast cancer. However, the detected rate of HPV16 varies with region. We will investigate HPV16 E6 expression in North China and explore the effects and mechanism of HPV16 E6 on breast cancer proliferation in this study. Methods. The expressions of HPV16 E6 and COX-2 in paraffin-embedded tissues of the invasive ductal breast cancer were detected by qPCR and IHC. The effects of HPV16 E6 on breast cancer proliferation were determined by function studies. The mechanism of HPV16 E6 in promoting breast cancer proliferation was explored by Western blot and Dual-Luciferase Reporter Assay. Results. HPV16 E6 was positive in 28% invasive ductal breast carcinoma in North China; HPV16 E6 promoted breast cancer proliferation. Inhibition of COX-2 by siCOX-2 or Celecoxib attenuated the proliferation of breast cancer cells with HPV16 E6 expression; and the upregulation of COX-2 could be suppressed by the inhibition of NF-κB activity. Conclusion. HPV16 E6 promotes breast cancer proliferation by activation of NF-κB signaling pathway and increase of COX-2 expression. COX-2 will be a potential target for HPV16 E6-associated breast cancer.