title: FHIT promotes the apoptosis of QBC939 by reducing the expression of cyclin D1.
abstract: OBJECTIVE
  The fragile histidine triad (FHIT) gene is a candidate tumor suppressor gene. Recent studies have found that FHIT protein is lost in digestive system neoplasms. However, there is limited information on the effect of FHIT on apoptosis and the regulation functions on cyclin D1 in cholangiocarcinoma.
  
  
  METHODS
  Eukaryotic expression plasmids with/without the FHIT gene were constructed and transfected into three groups in which cholangiocarcinoma cells were also divided. We observed the proliferation of cholangiocarcinoma by using the MTT method and flow cyclometry (FCM). Invasive ability was then determined via transwell chamber testing. In addition, to examine whether FHIT mRNA and protein expression were correlated with cyclin D1 expression, we used real-time RT-PCR and western blotting.
  
  
  RESULTS
  The absorbance (A490) was decreased significantly (p<0.05) according to MTT, showing that proliferation had been inhibited and the apoptosis ratio after transfecting had increased significantly (p<0.05). The amount of cells which passed the filter in the transwell chamber was significantly less (p<0.05). The expression of cyclin D1 mRNA and the protein was decreased from the original cell line (p<0.05).
  
  
  CONCLUSIONS
  The results suggest that increased FHIT gene activity can promote apoptosis of cholangiocarcinoma and reduce the expression level of cyclin D1.
authors.affiliation: Department of General Surgery, Affiliated Provincial Hospital of Anhui Medical University, Hefei, China. xupeng1228@gmail.com
authors.forename: Qiang
authors.initials: Q
authors.lastname: Huang
authors.forename: Fang
authors.initials: F
authors.lastname: Xie
authors.forename: Zhigang
authors.initials: Z
authors.lastname: Tang
authors.forename: Chenhai
authors.initials: C
authors.lastname: Liu
authors.forename: Cheng
authors.initials: C
authors.lastname: Wang
authors.forename: Yuanguo
authors.initials: Y
authors.lastname: Hu
authors.forename: Lujun
authors.initials: L
authors.lastname: Qiu
authors.forename: Shijie
authors.initials: S
authors.lastname: Wang
authors.forename: Hao
authors.initials: H
authors.lastname: You
authors.forename: Kai
authors.initials: K
authors.lastname: Zhu
authors.forename: Peng
authors.initials: P
authors.lastname: Xu
mesh_terms: D017766:Acid Anhydride Hydrolases / Q000235:genetics / Q000502:physiology*; D017209:Apoptosis; D001650:Bile Duct Neoplasms / Q000473:pathology*; D001653:Bile Ducts, Intrahepatic; D045744:Cell Line, Tumor; D018281:Cholangiocarcinoma / Q000473:pathology*; D019938:Cyclin D1 / Q000235:genetics / Q000502:physiology*; D006801:Humans; D009363:Neoplasm Proteins / Q000235:genetics / Q000502:physiology*; D012333:RNA, Messenger / Q000032:analysis; D014162:Transfection; D000099170:Bis(5'-adenosyl)triphosphatase
chemical_list: D017766:Acid Anhydride Hydrolases; D019938:Cyclin D1; D009363:Neoplasm Proteins; D012333:RNA, Messenger; D000099170:Bis(5'-adenosyl)triphosphatase; C530104:CCND1 protein, human