title: [Effects of Se-methylselenocysteine on biological behavior of and matrix metalloproteinase-2 expression in human breast cancer MDA-MB-231 cells].
abstract: OBJECTIVE
  Se-methylselenocysteine (MSC), a natural organoselenium compound, has functions on chemoprevention and treatment of many tumors, but the mechanism remains unclear. This study was to investigate the effects of MSC on the biological behavior of and matrix metalloproteinase-2 (MMP-2) expression in human breast cancer MDA-MB-231 cells.
  
  
  METHODS
  After treatment of MSC, the proliferation and apoptosis of MDA-MB-231 cells were detected with light microscope and Cell Counting Kit-8 (CCK-8), cell cycle and apoptosis were determined by flow cytometry, malignant phenotype was determined by soft agarose growth assay, and the expression of MMP-2 was determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. The concentration of MMP-2 protein in culture supernatant was measured with enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  MSC induced S phase arrest and apoptosis, inhibited the proliferation and colony formation of MDA-MB-231 cells. When treated with 50 mumol/L MSC for 48 h and 72 h, the mRNA levels of MMP-2 were up-regulated by 32.2% and 47.1%, whereas its protein levels were down-regulated by 42.4% and 50.8%, its concentrations in culture supernatant were down-regulated by 56.7% and 75.2%. When treated with 100 mumol/L MSC for 48 h and 72 h, the mRNA levels of MMP-2 were up-regulated by 52.6% and 61.3%, whereas its protein levels were down-regulated by 72.9% and 81.4%, and its concentrations in culture supernatant were down-regulated by 68.5% and 80.9%.
  
  
  CONCLUSIONS
  MSC could inhibit proliferation, and induce apoptosis and S phase arrest in MDA-MB-231 cells. MSC could also up-regulate the mRNA level of MMP-2 while down-regulate its protein level and secretion in the cells.
authors.affiliation: Department of Pathology and Pathophysiology, School of Basic Medical Science, Southeast University, Nanjing, Jiangsu, 210009, P. R. China.
authors.forename: Juan
authors.initials: J
authors.lastname: Wang
authors.forename: Nan-Lin
authors.initials: NL
authors.lastname: Jiao
authors.forename: Jie
authors.initials: J
authors.lastname: Zheng
mesh_terms: D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D003545:Cysteine / Q000031:analogs & derivatives* / Q000494:pharmacology; D005260:Female; D006801:Humans; D020778:Matrix Metalloproteinase 2 / Q000032:analysis / Q000235:genetics*; D016566:Organoselenium Compounds / Q000494:pharmacology*; D012333:RNA, Messenger / Q000032:analysis; D016196:S Phase / Q000187:drug effects; D017279:Selenocysteine / Q000031:analogs & derivatives
chemical_list: D016588:Anticarcinogenic Agents; D016566:Organoselenium Compounds; D012333:RNA, Messenger; D017279:Selenocysteine; C522361:MMP2 protein, human; D020778:Matrix Metalloproteinase 2; D003545:Cysteine; C002979:selenomethylselenocysteine