Abstract
Abstract Introduction: Protein Tyrosine Phosphatases (PTPs) are known as signalling molecules which affect cell growth, differentiation and oncogenic transformation. PTPs have been indicated in tumourigenesis and progression of various solid tumours. PTPRK, receptor-type protein tyrosine phosphatase kappa, has been shown to down-regulate transcriptional activity of beta-catenin and impact distribution of beta-catenin/E-cadherin complexes on cancer cell membrane. However, the role played by PTPRK in angiogenesis remains unknown. In present study, the effect of PTPRK knock-down on functions and tubule formation ability of HECV cells was investigated. (or In the present study, the effect of PTPRK on angiogenesis process was investigated.) Methods: anti-PTPRK ribozyme transgenes were constructed to knock-down PTPRK expression in vascular endothelial cells, HECV cells. The subsequent effect upon in vitro cell growth, adhesion, migration and microvascular tubule formation was examined using a variety of functional assays. Result: Knock-down PTPRK in HECV cells (HECVΔPTPRK) resulted in a decrease of cell growth in vitro. The growth rate of HECVΔPTPRK was 276.3±16.4, p=0.01 compared with HECVpEF (314.8±21.9) controls. However, knock-down of PTPRK in HECV cells increased cell motility. The cell migration distance of HECVΔPTPRK was 83.8±19.8μm, p=0.008 compared with HECVpEF (61.8±11.8μm) controls. No effect on cell adhesion by PTPRK knockdown was seen in HECVΔPTPRK (81.2±6.6), compared with HECVpEF control (78.8±15.6). Furthermore, knock-down of PTPRK suppressed tubule formation in HECV cells, the length of total tubules (μm) in HECVΔPTPRK was 2167.4±943.2, p<0.05 compared with HECVpEF (3130.6±386.9) control. Conclusion: Knock-down of PTPRK reduced the growth and tubule formation abilities of vascular endothelial cells. It suggests that PTPRK is pivotal regulator for angiogenic process. Further investigations are required to identify the downstream pathways involved in these impacts. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P2-05-05.
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