title: Protein tyrosine phosphatase µ (PTP µ or PTPRM), a negative regulator of proliferation and invasion of breast cancer cells, is associated with disease prognosis.
abstract: BACKGROUND
  PTPRM has been shown to exhibit homophilic binding and confer cell-cell adhesion in cells including epithelial and cancer cells. The present study investigated the expression of PTPRM in breast cancer and the biological impact of PTPRM on breast cancer cells.
  
  
  METHODS
  Expression of PTPRM protein and gene transcript was examined in a cohort of breast cancer patients. Knockdown of PTPRM in breast cancer cells was performed using a specific anti-PTPRM transgene. The impact of PTPRM knockdown on breast cancer was evaluated using in vitro cell models.
  
  
  RESULTS
  A significant decrease of PTPRM transcripts was seen in poorly differentiated and moderately differentiated tumours compared with well differentiated tumours. Patients with lower expression of PTPRM had shorter survival compared with those which had a higher level of PTPRM expression. Knockdown of PTPRM increased proliferation, adhesion, invasion and migration of breast cancer cells. Furthermore, knockdown of PTPRM in MDA-MB-231 cells resulted in increased cell migration and invasion via regulation of the tyrosine phosphorylation of ERK and JNK.
  
  
  CONCLUSIONS
  Decreased expression of PTPRM in breast cancer is correlated with poor prognosis and inversely correlated with disease free survival. PTPRM coordinated cell migration and invasion through the regulation of tyrosine phosphorylation of ERK and JNK.
authors.affiliation: Metastasis & Angiogenesis Research Group, Institute of Cancer and Genetics, Cardiff University School of Medicine, Cardiff, United Kingdom. sunp2@cf.ac.uk
authors.forename: Ping-Hui
authors.initials: PH
authors.lastname: Sun
authors.forename: Lin
authors.initials: L
authors.lastname: Ye
authors.forename: Malcolm D
authors.initials: MD
authors.lastname: Mason
authors.forename: Wen G
authors.initials: WG
authors.lastname: Jiang
mesh_terms: D001943:Breast Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000401:mortality / Q000473:pathology; D002448:Cell Adhesion; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D048049:Extracellular Signal-Regulated MAP Kinases / Q000235:genetics* / Q000378:metabolism; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D055785:Gene Knockdown Techniques; D006801:Humans; D048670:MAP Kinase Kinase 4 / Q000235:genetics* / Q000378:metabolism; D060787:Neoplasm Grading; D010766:Phosphorylation; D011379:Prognosis; D012333:RNA, Messenger / Q000378:metabolism; D054623:Receptor-Like Protein Tyrosine Phosphatases, Class 2 / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction; D016019:Survival Analysis
chemical_list: D012333:RNA, Messenger; D048049:Extracellular Signal-Regulated MAP Kinases; D048670:MAP Kinase Kinase 4; C516859:PTPRM protein, human; D054623:Receptor-Like Protein Tyrosine Phosphatases, Class 2