title: Bmi1 knockdown inhibits hepatocarcinogenesis.
abstract: Although Bmi1 is well established as one of the most commonly activated             oncogenes, the precise role of Bmi1 during hepatocarcinogenesis remains unclear.             In addition, Bmi1 provides a potential therapeutic target for the future treatment             of hepatocellular carcinoma (HCC). In this study, the expression of Bmi1 in HCC             tissues was evaluated by immunohistochemistry and western blot analysis. We found             that Bmi1 was much more highly expressed in HCC tissue compared to normal liver             tissue. The shRNA-mediated knockdown of Bmi1 was used to assess the effects of             Bmi1 in hepatocarcinogenesis. Bmi1 downregulation reduced cell growth and tumorsphere             formation in vitro. A cell cycle analysis using flow cytometry clarified that             Bmi1 knockdown blocked the cell cycle transition from the G0/G1 to the S phase.             Additionally, the Bmi1 knockdown led to reduced tumorigenicity in vivo. Furthermore,             Bmi1 expression enhanced the sensitivity of HCC to the therapeutic agent, sorafenib.             Taken together, the current results demonstrate that Bmi1 functions as a promoter             in cell proliferation and hepatocarcinogenesis, providing a potential therapeutic             target for the future treatment of HCC.
authors.affiliation: Department of Oncology, Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi, People's Republic of China.
authors.forename: Zhi-Ping
authors.initials: ZP
authors.lastname: Ruan
authors.forename: Rui
authors.initials: R
authors.lastname: Xu
authors.forename: Yi
authors.initials: Y
authors.lastname: Lv
authors.forename: Tao
authors.initials: T
authors.lastname: Tian
authors.forename: Wen-Juan
authors.initials: WJ
authors.lastname: Wang
authors.forename: Hui
authors.initials: H
authors.lastname: Guo
authors.forename: Ke-Jun
authors.initials: KJ
authors.lastname: Nan
mesh_terms: D000818:Animals; D017209:Apoptosis; D014408:Biomarkers, Tumor / Q000378:metabolism; D015153:Blotting, Western; D006528:Carcinoma, Hepatocellular / Q000235:genetics / Q000473:pathology / Q000517:prevention & control*; D002453:Cell Cycle; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic / Q000473:pathology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007124:Immunoenzyme Techniques; D008099:Liver / Q000473:pathology*; D008113:Liver Neoplasms / Q000235:genetics / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008875:Middle Aged; D048054:Mitogen-Activated Protein Kinase 7 / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D009367:Neoplasm Staging; D011379:Prognosis; D034741:RNA, Small Interfering / Q000235:genetics*; D015996:Survival Rate
chemical_list: D014408:Biomarkers, Tumor; D034741:RNA, Small Interfering; C481581:MAPK7 protein, human; D048054:Mitogen-Activated Protein Kinase 7