title: [The effects of p16 and Rb protein expression and NF-kappaB activity on hepatocarcinogenesis].
abstract: OBJECTIVE
  To study the relation between the expression of p16 protein and Rb (retinoblastoma) protein and the transcription activity of nuclear factor-kappaB (NF-kappaB) and their roles in hepatocarcinogenesis.
  
  
  METHODS
  p16 protein and Rb protein in 35 hepatocellular carcinoma (HCC) tissues and the peritumoral areas (more than 3 cm away from the tumor) were examined by Western blot analysis. The transcription activity of NF-kappaB in these tissues was detected by electrophoretic mobility shift assays (EMSA) and super-shift assays.
  
  
  RESULTS
  The expression rates of p16 protein in the HCC tissues and peritumoral areas were 37% (13/35) and 48% (17/35) respectively (P < 0.01). The expression rates of Rb protein in the HCC tissues and peritumoral areas were 34% (12/35) and 74% (26/35) respectively (P < 0.01). The emergence rates of NF-kappaB with transcription activity in the HCC tissues and peritumoral areas were 77% (27/35) and 85% (30/35) respectively (P > 0.05). Four out of the 10 (40%) HCC tissues expressing p16 protein and Rb protein simultaneously turned up NF-kappaB with transcription activity, while 18 out of the 20 (90%) HCC tissues not expressing both p16 and Rb proteins turned up NF-kappaB with transcription activity (P < 0.05). 13 out of the 17 (76%) peritumoral areas expressing two kinds of proteins simultaneously turned up NF-kappaB with transcription activity and the emergence rate of NF-kappaB with transcription activity in the peritumoral areas not expressing the two kinds of proteins was 89% (8/9) (P > 0.05).
  
  
  CONCLUSIONS
  Dysfunction of p16 is the early event of hepatocarcinogenesis and dysfunction of Rb is the later event in this course. There is a positive correlation between p16 protein and Rb protein in HCC tissues. The loss of expression of p16 and Rb proteins plays important roles in the carcinogenesis and progression of HCC by affecting NF-kappaB transcription activity which may prevent hepocyctes from apoptosis, besides disturbing cell cycle.
authors.affiliation: Department of General Surgery, Shanghai First People's Hospital, Shanghai Jiaotong University, Shanghai 200080, China.
authors.forename: Zhao-wen
authors.initials: ZW
authors.lastname: Wang
authors.forename: Zhi-hai
authors.initials: ZH
authors.lastname: Peng
authors.forename: Hua-mei
authors.initials: HM
authors.lastname: Tang
authors.forename: Guo-qiang
authors.initials: GQ
authors.lastname: Qiu
authors.forename: Tong-hai
authors.initials: TH
authors.lastname: Xing
authors.forename: Ming-zhi
authors.initials: MZ
authors.lastname: Yang
mesh_terms: D006528:Carcinoma, Hepatocellular / Q000209:etiology* / Q000378:metabolism; D019938:Cyclin D1 / Q000378:metabolism; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000032:analysis*; D005260:Female; D006801:Humans; D008113:Liver Neoplasms / Q000209:etiology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D016328:NF-kappa B / Q000378:metabolism*; D016160:Retinoblastoma Protein / Q000032:analysis*
chemical_list: D019941:Cyclin-Dependent Kinase Inhibitor p16; D016328:NF-kappa B; D016160:Retinoblastoma Protein; D019938:Cyclin D1