title: Gambogic acid induces mitochondria-dependent apoptosis by modulation of Bcl-2 and Bax in mantle cell lymphoma JeKo-1 cells.
abstract: OBJECTIVE
  To study the mechanisms in gambogic acid (GA) -induced JeKo-1 human Mantle Cell Lymphoma cell apoptosis in vitro.
  
  
  METHODS
  The proliferation of GA-treated JeKo-1 cells was measured by CCK-8 assay and Ki-67 immunocytochemical detection. Apoptosis, cell cycle and mitochondrial membrane potential were measured by flow cytometric analysis. Caspase-3, -8 and -9 were detected by colorimetric assay. Bcl-2 and Bax were analyzed by Western blotting.
  
  
  RESULTS
  GA inhibited cell growth in a time- and dose- dependent manner. GA induces apoptosis in JeKo-1 cells but not in normal bone marrow cells, which was involved in reducing the membrane potential of mitochondria, activating caspases-3, -8 and -9 and decreasing the ratio of Bcl-2 and Bax without cell cycle arresting.
  
  
  CONCLUSIONS
  GA induced apoptosis in human MCL JeKo-1 cells by regulating Bcl-2/Bax and activating caspase-3, -8 and -9 via mitochondrial pathway without affecting cell cycle.
authors.affiliation: Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210038, PR China;
authors.forename: Jingyan
authors.initials: J
authors.lastname: Xu
authors.forename: Min
authors.initials: M
authors.lastname: Zhou
authors.forename: Jian
authors.initials: J
authors.lastname: Ouyang
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.forename: Qiguo
authors.initials: Q
authors.lastname: Zhang
authors.forename: Yong
authors.initials: Y
authors.lastname: Xu
authors.forename: Yueyi
authors.initials: Y
authors.lastname: Xu
authors.forename: Qian
authors.initials: Q
authors.lastname: Zhang
authors.forename: Xihui
authors.initials: X
authors.lastname: Xu
authors.forename: Hui
authors.initials: H
authors.lastname: Zeng
keywords: Bax; Bcl-2; Gambogic acid; JeKo-1 cells; caspase-3; caspase-8; caspase-9; cell cycle arrest, apoptosis; membrane potential of mitochondria