title: Protein tyrosine phosphatase kappa (PTPRK) is a negative regulator of adhesion and invasion of breast cancer cells, and associates with poor prognosis of breast cancer.
abstract: OBJECTIVE
  Receptor-like protein tyrosine phosphatase kappa (PTPRK) has been shown to exhibit homophilic binding. It is a putative tumour suppressor in primary central nervous system lymphomas and colorectal cancer. The present study investigated the expression of PTPRK in breast cancer and the biological impact of PTPRK on breast cancer cells.
  
  
  METHODS
  Expression of PTPRK protein and gene transcript was examined in a cohort of breast cancer patients. The association of PTPRK transcript level and pathological and clinical aspects was then analysed. Knockdown of PTPRK in breast cancer cells was performed using a specific anti-PTPRK transgene. The impact of PTPRK knockdown on breast cancer cells was investigated using in vitro cell function assays.
  
  
  RESULTS
  Lower levels of PTPRK transcripts were seen in the advanced breast cancer. The reduced PTPRK transcript levels were associated with poor prognosis of the disease. PTPRK transcript levels were decreased in the primary tumours of patients who died from breast cancer or had metastases. Patients with lower expression of PTPRK had shorter survival compared with those higher expression levels of PTPRK. Knockdown of PTPRK resulted in increased proliferation, adhesion, invasion, and migration of breast cancer cells in vitro.
  
  
  CONCLUSIONS
  Decreased expression of PTPRK in breast cancer is correlated with poor prognosis. PTPRK is a negative regulator of adhesion, invasion, migration, and proliferation of breast cancer cells. This suggests that PTPRK is a potential tumour suppressor in breast cancer.
authors.affiliation: Metastasis and Angiogenesis Research Group, Institute of Cancer and Genetics, Cardiff University School of Medicine, Cardiff CF14 4XN, UK. 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 / Q000201:enzymology* / Q000401:mortality / Q000473:pathology; D018270:Carcinoma, Ductal, Breast / Q000201:enzymology* / Q000401:mortality / Q000556:secondary; D018275:Carcinoma, Lobular / Q000201:enzymology* / Q000401:mortality / Q000556:secondary; D002448:Cell Adhesion; D002465:Cell Movement; D049109:Cell Proliferation; D018572:Disease-Free Survival; D005260:Female; D015870:Gene Expression; D055785:Gene Knockdown Techniques; D006801:Humans; D053208:Kaplan-Meier Estimate; D008207:Lymphatic Metastasis; D061986:MCF-7 Cells; D009361:Neoplasm Invasiveness; D054623:Receptor-Like Protein Tyrosine Phosphatases, Class 2 / Q000235:genetics / Q000378:metabolism*
chemical_list: C489852:PTPRK protein, human; D054623:Receptor-Like Protein Tyrosine Phosphatases, Class 2
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