title: [The effect of leptin and its mechanisms on the migration and invasion of human breast cancer MCF-7 cells].
abstract: OBJECTIVE
  To investigate the effect and the relevant molecular mechanisms of leptin on the migration and invasion of human breast cancer MCF-7 cells.
  
  
  METHODS
  The expression of OB-R in MCF-7 cells was measured by RT-PCR and Western blotting. The effects of leptin (100 ng/mL) on the the phosphorylation of a few key cell signaling proteins, p-ERK1/2, p-STAT3, p-AKT in MCF-7 cells were examined by Western blotting. Cell scratch assay and Transwell(TM); assay were utilized to measure the effects of leptin on the migration and invasion capability of MCF-7 cells, respectively. The effects of leptin on the mRNA and protein expression of matrix metalloproteinas 9 (MMP-9) and transforming growth factor β (TGF-β) were measured by RT-PCR and Western blotting.
  
  
  RESULTS
  Both OB-Rb and OB-Rt were expressed in MCF-7 cells. This indicated that leptin may have significant activities in MCF7 cells. Indeed, leptin increased the phosphorylation of p-ERK1/2, p-STAT3, and p-AKT in MCF-7 cells (P < 0.05). Further, leptin promoted migration and invasion of MCF-7 cells, which were attenuated by the JAK/STAT inhibitor AG490 (50 μmol/L), and the PI3K/AKT inhibitor LY294002 (10 μmol/L) (P < 0.05). Similarly, leptin also increased the mRNA and protein expression of MMP-9 and TGF-β, and these effects were blocked by AG490 and LY294002 as well (P < 0.05).
  
  
  CONCLUSIONS
  Leptin promoted the migration and invasion capabilities of MCF-7 cells. These activities may be achieved by the upregulation of MMP-9 and TGF-β through JAK/STAT and PI3K/AKT signaling pathways.
authors: Key Laboratory of Laboratory Medical Diagnostics, Ministry of Eduction, Chongqing Medical University, Chongqing 400016, China.
authors: Lin
authors: L
authors: Wang
authors: Hong
authors: H
authors: Cao
authors: Xueli
authors: X
authors: Pang
authors: Kuangfa
authors: K
authors: Li
authors: Weiqi
authors: W
authors: Dang
authors: Hao
authors: H
authors: Tang
authors: Tingmei
authors: T
authors: Chen
mesh_terms: D001943:Breast Neoplasms / Q000473:pathology*; D002465:Cell Movement / Q000187:drug effects*; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D006801:Humans; D020738:Leptin / Q000494:pharmacology*; D061986:MCF-7 Cells; D020780:Matrix Metalloproteinase 9 / Q000235:genetics; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D009361:Neoplasm Invasiveness; D010750:Phosphoproteins / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D054411:Receptors, Leptin / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000235:genetics
chemical_list: D020738:Leptin; D010750:Phosphoproteins; D054411:Receptors, Leptin; D050796:STAT3 Transcription Factor; D016212:Transforming Growth Factor beta; D051057:Proto-Oncogene Proteins c-akt; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D020780:Matrix Metalloproteinase 9