Ste20-like kinase is upregulated in glioma and induces glioma invasion

Neoplasma. 2018;65(2):185-191. doi: 10.4149/neo_2018_170318N193.

Abstract

The malignant development and poor prognosis of gliomas are associated with a high degree of invasion and a high recurrence rate. However, the molecular mechanism underlying the invasiveness of glioma remains to be elucidated. Ste20- like kinase (SLK) is one of the members of the Ste20 family, which has been implicated in cellular migration and invasion. In this study, we intended to explore the expression of SLK significantly related to clinicopathologic stages of gliomas. Immunohistochemical staining and western blot analysis demonstrated that SLK was highly expressed in human glioma tissues and cell lines. Kaplan-Meier analysis revealed that poor survival was associated with high SLK expression. The inhibition of SLK by RNA interference significantly suppressed the invasion ability of glioma, and on protein level, knock- down of SLK leaded to an up-regulation of E-cadherin and a down-regulation of Vimentin in glioma cells. Collectively, this research shed light on mechanisms of invasion and progression of malignant gliomas and suggested that SLK may be a potential therapeutic strategy for glioma.

Keywords: E-cadherin; SLK; glioma; invasion knock-down..

MeSH terms

  • Antigens, CD / genetics
  • Antigens, CD / metabolism
  • Brain Neoplasms / genetics
  • Brain Neoplasms / pathology*
  • Cadherins / genetics
  • Cadherins / metabolism
  • Cell Line, Tumor
  • Cell Movement
  • Down-Regulation
  • Gene Expression Regulation, Neoplastic
  • Glioma / genetics
  • Glioma / pathology*
  • Humans
  • Neoplasm Invasiveness
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • RNA Interference
  • Vimentin / genetics
  • Vimentin / metabolism

Substances

  • Antigens, CD
  • CDH1 protein, human
  • Cadherins
  • Vimentin
  • SLK protein, human
  • Protein Serine-Threonine Kinases