Downregulation of urokinase-type plasminogen activator receptor (uPAR) induces caspase-mediated cell death in human glioblastoma cells

Niranjan Yanamandra, Santhi D. Konduri, Sanjeeva Mohanam, Dzung H. Dinh, William C. Olivero, Meena Gujrati, Garth L. Nicolson, Mandri Obeyeseke, Jasti S. Rao

Research output: Contribution to journalArticle

Abstract

Urokinase-type plasminogen activator receptors (uPARs) play an important role in tumor invasion by localizing degradative enzymes at the invasive zone. Our previous studies with human glioblastoma cell line SNB 19 expressing AS-uPAR stable tranfectant lose their invasive properties when injected in vivo. The aim of the present study is to investigate whether the inhibition of tumor formation is due to apoptosis. Apoptosis is a highly conserved cell suicide program essential for development and tissue homeostasis of all metazoan organisms. Key to the apoptotic program is a family of cystein proteases termed caspases, which are important for execution of apoptosis by cleavage of essential cellular proteins. We found loss of mitochondrial transmembrane potential, release of cytochrome C from mitochondria and subsequent activation of Caspase-9 in SNB19 AS-uPAR cells compared to parental and vector controls. Our results indicate that suppression of uPAR results in apoptosis and suggest that Caspase-9 dependent apoptosis plays an important role in SNB19 AS-uPAR-induced apoptosis.

Original languageEnglish (US)
Pages (from-to)611-615
Number of pages5
JournalClinical and Experimental Metastasis
Volume18
Issue number7
DOIs
StatePublished - Dec 1 2000

Keywords

  • Antisense
  • Caspases
  • Glioblastoma
  • Oligonucleotides
  • uPAR

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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