title: [Effect of JIP on the proliferation and apoptosis of nasopharyngeal carcinoma cells].
abstract: OBJECTIVE
  Previous studies showed that JNK signaling pathway activated by LMP1 plays an important role in carcinogenesis of nasopharyngeal carcinoma (NPC). JNK interacting protein (JIP) can inhibit JNK signaling pathway in NPC cell. This study was designed to elucidate the effect of JIP on the proliferation and apoptosis of NPC cells.
  
  
  METHODS
  After treatment with JIP at different concentrations and time points, the number of proliferating cells were determined by MTT assay; the ability of proliferation of NPC cells was measured by the rate of cloning formation; cell cycle and the apoptotic rate of NPC cells was assayed by flow cytometry.
  
  
  RESULTS
  1. MTT assay showed that cell proliferation was significantly inhibited by JIP in a dose- and time-dependent manner. After treatment with JIP for 24, 48, and 72 hours, the rate of survival cells were 77.8%, 59.2%, and 61.8%, respectively. 2. The number and volume of colonies were decreased after transfection with JIP. 3. The number of cells in S phase was decreased from 25.87% to 19.96%, and the number of cells in G0/G1 phase was elevated from 66.24% to 71.89% after treatment with JIP. 4. In contrast to the control group, the 24 hours apoptotic rate was elevated from 1.25% to 8.25% (about 6.6 times); the 48 hours apoptotic rate was elevated from 1.04% to 31.45% (about 30 times).
  
  
  CONCLUSIONS
  The results demonstrated that JIP inhibit the growth of nasopharyngeal carcinoma through arresting the cell cycle at G1/S checkpoint and triggering the apoptosis of cells. Data suggest that JIP is a potent molecular drug for the treatment of the patients with nasopharyngeal carcinoma.
authors.affiliation: Institute of Cancer Research, Xiangya School of Medicine, Central South University, Changsha 410078, P. R. China.
authors.forename: Zhi
authors.initials: Z
authors.lastname: Hu
authors.forename: Yong-guang
authors.initials: YG
authors.lastname: Tao
authors.forename: Li-fang
authors.initials: LF
authors.lastname: Yang
authors.forename: Fa-qing
authors.initials: FQ
authors.lastname: Tang
authors.forename: Fei-jun
authors.initials: FJ
authors.lastname: Luo
authors.forename: Liang
authors.initials: L
authors.lastname: Zeng
authors.forename: Wei
authors.initials: W
authors.lastname: Yi
authors.forename: Ya
authors.initials: Y
authors.lastname: Cao
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D002453:Cell Cycle / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D045744:Cell Line, Tumor; D003114:Colony-Forming Units Assay; D004305:Dose-Response Relationship, Drug; D006801:Humans; D009303:Nasopharyngeal Neoplasms / Q000378:metabolism / Q000473:pathology*; D014162:Transfection; D014763:Viral Matrix Proteins / Q000378:metabolism
chemical_list: D048868:Adaptor Proteins, Signal Transducing; C037662:EBV-associated membrane antigen, Epstein-Barr virus; C490666:MAPK8IP1 protein, human; D014763:Viral Matrix Proteins