title: Crocetin induces cytotoxicity in colon cancer cells via p53-independent mechanisms.
abstract: OBJECTIVE
  Crocin has been proposed as a promising candidate for cancer chemoprevention. The purpose of this investigation was to investigate the chemopreventive action and the possible mechanisms of crocin against human colon cancer cells in vitro.
  
  
  METHODS
  Cell proliferation was examined using MTT assay and the cell cycle distribution fractions were analyzed using flow cytometric analysis after propidium iodide staining. Apoptosis was detected using the TUNEL Apoptosis Detection Kit with laser scanning confocal microscope. DNA damage was assessed using the alkaline single-cell gel electrophoresis assay, while expression levels of p53, cdk2, cyclin A and P21 were examined by Western blot analysis.
  
  
  RESULTS
  Treatment of SW480 cells with crocetin (0.2, 0.4, 0.8 mmol/L) for 48 h significantly inhibited their proliferation in a concentration-dependent manner. Crocetin (0.8 mmol/L) significantly induced cell cycle arrest through p53-independent mechanisms accompanied by P21 induction. Crocetin (0.8 mmol/L) caused cytotoxicity in the SW480 cells by enhancing apoptosis and decreasing DNA repair capacity in a time-dependent manner.
  
  
  CONCLUSIONS
  This report provides evidence that crocetin is a potential anticancer agent, which may be used as a chemotherapeutic drug.
authors.affiliation: Clinical Laboratory Medicine Center, The Second People's Hospital of Jingmen, Jingmen, China. wangfan19840303@126.com
authors.forename: Cai-Yan
authors.initials: CY
authors.lastname: Li
authors.forename: Wen-Feng
authors.initials: WF
authors.lastname: Huang
authors.forename: Qun-Li
authors.initials: QL
authors.lastname: Wang
authors.forename: Fan
authors.initials: F
authors.lastname: Wang
authors.forename: E
authors.initials: E
authors.lastname: Cai
authors.forename: Bing
authors.initials: B
authors.lastname: Hu
authors.forename: Jia-Cheng
authors.initials: JC
authors.lastname: Du
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.forename: Rong
authors.initials: R
authors.lastname: Chen
authors.forename: Xiao-Jing
authors.initials: XJ
authors.lastname: Cai
authors.forename: Jing
authors.initials: J
authors.lastname: Feng
authors.forename: Hui-Hui
authors.initials: HH
authors.lastname: Li
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D002338:Carotenoids / Q000494:pharmacology*; D002453:Cell Cycle / Q000187:drug effects; D018797:Cell Cycle Proteins / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects*; D003110:Colonic Neoplasms / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D020552:Comet Assay; D004249:DNA Damage / Q000187:drug effects*; D005434:Flow Cytometry; D006801:Humans; D051379:Mice; D009154:Mutation / Q000235:genetics; D041681:NIH 3T3 Cells; D014407:Tumor Cells, Cultured; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*; D014801:Vitamin A / Q000031:analogs & derivatives; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D016588:Anticarcinogenic Agents; D018797:Cell Cycle Proteins; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; C487773:trans-sodium crocetinate; D014801:Vitamin A; D002338:Carotenoids