title: Bmi-1 promotes the chemoresistance, invasion and tumorigenesis of pancreatic cancer cells.
abstract: OBJECTIVE
  The polycomb protein Bmi-1 plays oncogenic roles in various cancers. Here we aimed to investigate the contribution of Bmi-1 on the malignant behaviors of pancreatic cancer such as chemoresistance, invasion and tumorigenesis.
  
  
  RESULTS
  The MTT cell proliferation assay showed that shRNA mediated Bmi-1 knockdown and enhanced the chemosensitivity of pancreatic cancer cells to gemcitabine. The transwell invasion assay showed that Bmi-1 knockdown inhibited the invasion of pancreatic cancer cells in vitro. Notably, the reduced abilities of chemoresistance and invasion were associated with the transition from the mesenchymal phenotype to the epithelial phenotype of pancreatic cancer cells. Moreover, Bmi-1 knockdown led to the inhibition of the PI3K-Akt pathway and disrupted the sphere-forming abilities of pancreatic cancer cells. A nude mouse xenograft experiment demonstrated that pancreatic cancer cells depleted of Bmi-1 showed weak tumorigenicity in vivo.
  
  
  CONCLUSIONS
  Our data suggest that Bmi-1 plays an important role in the progression of pancreatic cancer and represents a novel target for antitumor therapy of pancreatic cancer.
authors.affiliation: Pancreatic Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.
authors.forename: Tao
authors.initials: T
authors.lastname: Yin
authors.forename: Hongji
authors.initials: H
authors.lastname: Wei
authors.forename: Zhenwei
authors.initials: Z
authors.lastname: Leng
authors.forename: Zhiyong
authors.initials: Z
authors.lastname: Yang
authors.forename: Shanmiao
authors.initials: S
authors.lastname: Gou
authors.forename: Heshui
authors.initials: H
authors.lastname: Wu
authors.forename: Gang
authors.initials: G
authors.lastname: Zhao
authors.forename: Xiaoqing
authors.initials: X
authors.lastname: Hu
authors.forename: Chunyou
authors.initials: C
authors.lastname: Wang
mesh_terms: D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D019008:Drug Resistance, Neoplasm / Q000235:genetics*; D005260:Female; D055785:Gene Knockdown Techniques; D006801:Humans; D051379:Mice; D008819:Mice, Nude; D009361:Neoplasm Invasiveness / Q000235:genetics / Q000473:pathology; D009687:Nuclear Proteins / Q000037:antagonists & inhibitors / Q000172:deficiency / Q000502:physiology*; D010190:Pancreatic Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D063150:Polycomb Repressive Complex 1; D011518:Proto-Oncogene Proteins / Q000037:antagonists & inhibitors / Q000172:deficiency / Q000502:physiology*; D012097:Repressor Proteins / Q000037:antagonists & inhibitors / Q000172:deficiency / Q000502:physiology*; D014407:Tumor Cells, Cultured; D023041:Xenograft Model Antitumor Assays / Q000379:methods
chemical_list: C489421:Bmi1 protein, mouse; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; D012097:Repressor Proteins; D063150:Polycomb Repressive Complex 1