Abstract
Cervical carcinoma is the main cause of cancer-related mortality in women and is correlated with more than 15 risk cofactors, including infection of cervical cells with high-risk types of HPV (hrHPV). Indeed, both aberrant methylation of the RASSF1A promoter and hrHPV infection are often observed in cervical carcinomas. The purpose of our meta-analysis was to evaluate the role of RASSF1A promoter methylation and hrHPV infection in cervical cancer. Our meta-analysis involved 895 cervical cancer patients and 454 control patients from 15 studies. Our results suggested that RASSF1A promoter hypermethylation increased the risk of cervical cancer (OR=9.77, 95%CI=[3.06, 31.26], P=0.0001, I2=78%). By grouping cases according to cancer subtypes, we found that HPV infection was higher in cervical squamous cell carcinomas (SCCs) than in cervical adenocarcinomas/ adenosquamous cancers (ACs/ASCs) (OR=4.00, 95%CI=[1.41, 11.30], P=0.009, I2=55%). Interestingly, HPV infection tended to occur in cervical cancers with relatively low levels of RASSF1A promoter methylation (OR=0.59, 95%CI=[0.36, 0.99], P=0.05, I2=0%). Our study provides evidence of a possible interaction between HPV infection and RASSF1A promoter methylation in the development of cervical cancers.
Highlights
Cervical cancers remain the third leading cause of genital system cancer-related mortality in women, despite the widespread application of screening methods for the prevention and early detection of cervical cancer
RASSF1A Promoter Hypermethylation and Oncogenic HPV Infection in Invasive Cervical Cancer: a Meta-analysis a total of 15 studies, representing 895 cervical cancer analysis by specific cervical cancer subtypes showed that cases and 454 corresponding controls, for inclusion in aberrant RASSF1A promoter hypermethylation tended to our subsequent meta-analyses (Figure 1)
The RASSF1A promoter methylation frequency ranged in squamous cell carcinomas (SCCs), the difference did from 0% to 73.85% in cervical cancer not reach statistical significance (OR=0.48, 95%CI=(0.15, tissues and from 0% to 41.18% in the paired 1.53), P=0.21, I2=80%, Figure 3)
Summary
Cervical cancers remain the third leading cause of genital system cancer-related mortality in women, despite the widespread application of screening methods for the prevention and early detection of cervical cancer. A majority of the women infected with HPV do not develop cervical cancer, and 90% of HPV infections usually resolve on their own within 2 years. Other complex genetic and epigenetic alterations might cooperate to drive the development of cervical cancers. In addition to cancer-related genetic mutations (Zhu et al, 2014), epigenetic alterations without changes in gene sequences, such as promoter hypermethylation, are relatively common events in many human cancers (Bird, 1986; Jiang et al, 2014a; Jiang et al, 2014b). Several tumor suppressor genes (TSGs) have been found to be frequently inactivated by promoter hypermethylation and linked with the pathogenesis and progression of cervical cancers (Cheung et al, 2004; Jha et al, 2012). Aberrant methylation of the RASSF1A promoter was often observed in cervical carcinomas (Yu et al, 2003; Maliukova et al, 2004)
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