title: Bmi1 gene silencing inhibits the proliferation and invasiveness of human             hepatocellular carcinoma cells and increases their sensitivity to 5-fluorouracil.
abstract: The Bmi1 gene has been reported to play important roles in cancer initiation             and progression. The aim of this study was to investigate the effects of RNA interference             (RNAi)-mediated silencing of Bmi1 gene expression on the proliferation and invasiveness             of hepatocellular carcinoma (HCC) cells and on the efficacy of chemotherapy in             HCC patients. The Bmi1 gene was silenced by Bmi1-siRNA (small interfering RNA)             in the human HCC cell lines HepG2 and Bel-7402, and the gene expression levels             were assayed by real-time quantitative reverse transcription-polymerase chain             reaction (qRT-PCR) and western blotting. The proliferation and migration of Bmi1-silenced             tumor cells and their sensitivity to 5-FU treatment were determined by Cell Counting             Kit-8 (CCK-8), transwell assays and 4',6-diamidino-2-phenylindole (DAPI) staining             and flow cytometry, respectively. Bmi1-siRNA inhibited the Bmi1 expression at             both the mRNA and protein levels in HCC cells. Proliferation and migration of             HCC cells treated with Bmi1-siRNA was significantly lower compared to that of             the control cells. Moreover, Bmi1 gene silencing increased the percentage of apoptotic             cells treated by 5-FU and decreased the IC50 values of 5-FU to a greater extent.             Downregulation of the Bmi1 gene by RNAi can inhibit the proliferation and invasivesness             of HCC cells and increase their sensitivity to 5-FU treatment.
authors.affiliation: Department of Hepato-Pancreato-Biliary Surgery, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, Guangdong Province, PR China.
authors.forename: Rui
authors.initials: R
authors.lastname: Zhang
authors.forename: Lei-Bo
authors.initials: LB
authors.lastname: Xu
authors.forename: Xiu-Jing
authors.initials: XJ
authors.lastname: Yue
authors.forename: Xian-Huan
authors.initials: XH
authors.lastname: Yu
authors.forename: Jie
authors.initials: J
authors.lastname: Wang
authors.forename: Chao
authors.initials: C
authors.lastname: Liu
mesh_terms: D015703:Antigens, CD / Q000378:metabolism; D000964:Antimetabolites, Antineoplastic / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D015820:Cadherins / Q000378:metabolism; D006528:Carcinoma, Hepatocellular / Q000188:drug therapy* / Q000378:metabolism; D002465:Cell Movement; D049109:Cell Proliferation; D019008:Drug Resistance, Neoplasm; D005472:Fluorouracil / Q000494:pharmacology*; D055785:Gene Knockdown Techniques; D056945:Hep G2 Cells; D006801:Humans; D008113:Liver Neoplasms / Q000188:drug therapy* / Q000378:metabolism; D063150:Polycomb Repressive Complex 1 / Q000235:genetics* / Q000378:metabolism; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000235:genetics; D014746:Vimentin / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D000964:Antimetabolites, Antineoplastic; C069077:BMI1 protein, human; C513384:CDH1 protein, human; C050361:CDH2 protein, human; D015820:Cadherins; D034741:RNA, Small Interfering; D014746:Vimentin; D063150:Polycomb Repressive Complex 1; D005472:Fluorouracil