title: [Interaction between folate and the expression of human papillomavirus 16 E6/E7 mRNA in the progression of cervix carcinogenesis].
abstract: OBJECTIVE
  To explore the interaction between folate and the expression of HPV16 E6/E7 mRNA in the progression of cervix carcinogenesis.
  
  
  METHODS
  Subjects were selected from the participants who were diagnosed pathologically, including 64 patients with cervical squamous cell carcinoma (SCC), 55 patients with low-grade cervical intraepithelial neoplasm (CIN1), 55 patients with high-grade cervical intraepithelial neoplasm (CIN2+) and 80 with normal cervix (NC). The levels of serum folate and RBC folate were detected by microbiological assay, and the expression levels of HPV16 E6/E7 mRNA were measured, using the real-time polymerase chain reaction (real-time PCR). Data was analyzed by methods as chi-square test, analysis of variance (ANOVA), Welch test, Kruskal-Wallis H test and ordinal logistic regression. Spearman correlation was tested using the SPSS statistical software (version 16.0) while the interaction effects were evaluated by additive model.
  
  
  RESULTS
  There was a positive correlation seen between the serum folate and RBC folate (r=0.41, P<0.001). The levels of serum folate and RBC folate decreased gradually along with the severity of cervical lesions (χ(2)=32.71, P<0.001; χ(2)=16.32, P<0.001). The expression levels of HPV16 E6/E7 mRNA increased gradually with the severity of cervical lesions (χ(2)=30.11, P<0.001; χ(2)=38.99, P<0.001). There was a negative correlation between the levels of RBC folate, expression levels of HPV16 E6 (E6: r=-0.14, P=0.009) and HPV16 E7 mRNA (E7: r=-0.21, P=0.001), respectively. Both RBC folate deficiency and HPV16 E6/E7 mRNA high expression showed additive interaction in CIN1,CIN2+ and SCC.
  
  
  CONCLUSIONS
  Folate deficiency and high expression of HPV16 E6/E7 mRNA might increase the risk of cervical cancer and cervix precancerous lesions, and having a synergistic action in the progression of cervix carcinogenesis.
authors.affiliation: Department of Epidemiology, School of Public Health, Shanxi Medical University, Taiyuan 030001, China.
authors.forename: J
authors.initials: J
authors.lastname: Nan
authors.forename: L
authors.initials: L
authors.lastname: Ding
authors.forename: X Z
authors.initials: XZ
authors.lastname: Liu
authors.forename: J
authors.initials: J
authors.lastname: Li
authors.forename: T T
authors.initials: TT
authors.lastname: Wu
authors.forename: X
authors.initials: X
authors.lastname: Chen
authors.forename: J T
authors.initials: JT
authors.lastname: Wang
mesh_terms: D002471:Cell Transformation, Neoplastic; D018450:Disease Progression; D005260:Female; D005492:Folic Acid; D052162:Human papillomavirus 16; D006801:Humans; D009856:Oncogene Proteins, Viral; D050725:Papillomavirus E7 Proteins; D030361:Papillomavirus Infections; D012333:RNA, Messenger; D060888:Real-Time Polymerase Chain Reaction; D012097:Repressor Proteins; D002583:Uterine Cervical Neoplasms
chemical_list: C068651:E6 protein, Human papillomavirus type 16; D009856:Oncogene Proteins, Viral; D050725:Papillomavirus E7 Proteins; D012333:RNA, Messenger; D012097:Repressor Proteins; C059731:oncogene protein E7, Human papillomavirus type 16; D005492:Folic Acid