title: [Experimental study on anti-tumor effect and mechanism of green tea extract].
abstract: OBJECTIVE
  To explore anti-cancer effect and mechanism of green tea extract (GTE) in three human oral squamous carcinoma cell lines (CAL-27, SCC-25 and KB).
  
  
  METHODS
  The cell lines were in vitro cultured and its growth inhibition was detected by MTT. After screening most sensitive cell line, effect of GTE on CAL-27 cell cycle was analyzed by flow cytometry. The protein expression of GTE on CAL-27 cell strain was determined by protein chip technique. The protein expression of CDK4, CDK6, and p-PDK1 was verified by using Western blot.
  
  
  RESULTS
  Compared with the control group, the inhibition rate on CAL-27 increased significantly after treated by 50, 100, 200, and 400 μg/mL GTE; the inhibition rate on KB increased after treated by 100, 200, and 400 μg/mL GTE; the inhibition rate on SCC-25 increased after treated by 25, 50, 100, 200, and 400 μg/mL GTE, all with statistical difference and in dose dependant manner (P < 0.01). Flow cytometric analysis showed that, when compared with the control group, 50 μg/mL GTE arrested CAL-27 cells in the G2/M phase (P < 0.05), and 100 μg/mL GTE arrested CAL-27 cells in the G2/M phase with concurrent decreased cells in the G0/G1 phase (P < 0.01). Totally 107 proteins were analyzed by protein chip technique. After treated by GTE, a total of 13 proteins significantly changed in CAL-27 cell line. Western blot showed that 25, 50, and 100 μg/mL GTE inhibited the expression of phopho-phosphoinositide-dependent protein kinase 1 (p-PDK1), cyclin-dependent kinase 4 (CDK4), and CDK6 of CAL-27 cell line with statistical difference (P < 0.05). The higher the drug concentration, the higher the inhibition rate (P < 0.05).
  
  
  CONCLUSIONS
  GTE could inhibit the proliferation of different human oral squamous carcinoma cell lines. CAL-27 is a sensitive cell line. GTE significantly affected EGFR and Notch signal network, and influenced changes of cell cycle related protein expression levels through the aforesaid channels, resulting in cell cycle arrest in S and G2/M phases.
authors.affiliation: First Hospital of Jilin University, Changchun, China.
authors.forename: Xiao-Liang
authors.initials: XL
authors.lastname: Liu
authors.forename: Huan-Qiu
authors.initials: HQ
authors.lastname: Liu
authors.forename: Ji
authors.initials: J
authors.lastname: Li
authors.forename: Le
authors.initials: L
authors.lastname: Yang
authors.forename: Xin
authors.initials: X
authors.lastname: Zhao
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology* / Q000627:therapeutic use; D000975:Antioxidants; D002294:Carcinoma, Squamous Cell; D002453:Cell Cycle; D045744:Cell Line, Tumor; D051358:Cyclin-Dependent Kinase 4; D004365:Drugs, Chinese Herbal / Q000494:pharmacology* / Q000627:therapeutic use; D016193:G1 Phase; D006801:Humans; D009062:Mouth Neoplasms; D013662:Tea
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D000975:Antioxidants; D004365:Drugs, Chinese Herbal; D013662:Tea; C495900:CDK4 protein, human; D051358:Cyclin-Dependent Kinase 4