Chloroquine inhibits the malignant phenotype of glioblastoma partially by suppressing TGF-beta

Invest New Drugs. 2015 Oct;33(5):1020-31. doi: 10.1007/s10637-015-0275-x. Epub 2015 Aug 15.

Abstract

Background: Glioblastoma (GBM), the most common and aggressive primary brain tumor, is characterized by excessive brain infiltration which prevents the complete surgical resection. These tumors also display treatment non-compliance and responses to standard therapy are invariably transient; consequently, the prognosis barely exceeds 14 months and recurrence is inevitable. Accordingly, several new treatment strategies have been studied. One such option is the use of chloroquine (CQ), a lysosomotropic weak base and renowned antimalarial drug, that has shown promising results in several pre-clinical studies. In this paper, we investigate the efficiency of CQ to hinder the malignant phenotype of GBM, namely extensive proliferation, invasion and radio-resistance.

Results: In cell cycle analysis, proliferation assays and immunofluorescence, CQ treatments halved proliferation of primary cultures from GBM specimens and GBM cell lines (U-373 MG et U-87 MG). Gelatin zymography and Matrigel(TM)-coated transwell invasion assays also revealed a 50 % CQ induced inhibition of MMP-2 activity and GBM invasion. Concomitant treatment with CQ and radiation also radiosensitized GBM cells as shown by an accumulation in the G2/M phase, increased cell death and reduced clonogenic formation. Moreover, radiation-induced invasion was considerably restrained by CQ. We also observe that these effects are owed to CQ-induced inhibition of TGF-β secretion and signaling pathway, a predominant growth factor in GBM progression.

Conclusion: These results suggest that CQ, alone or as an adjuvant therapeutic, could be used to inhibit the GBM malignant phenotype and could benefit GBM afflicted patients.

Keywords: Cellular proliferation and invasion; Chloroquine; Glioblastoma; Radioresistance; Transforming growth factor-beta.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Brain Neoplasms / drug therapy*
  • Brain Neoplasms / pathology
  • Cell Cycle
  • Cell Death
  • Cell Line, Tumor
  • Cell Proliferation
  • Chemoradiotherapy
  • Chloroquine / pharmacology*
  • Fluorescent Antibody Technique
  • Glioblastoma / drug therapy*
  • Glioblastoma / pathology
  • Humans
  • Matrix Metalloproteinase 2 / drug effects
  • Phenotype
  • Real-Time Polymerase Chain Reaction
  • Signal Transduction
  • Transforming Growth Factor beta / antagonists & inhibitors*

Substances

  • Transforming Growth Factor beta
  • Chloroquine
  • Matrix Metalloproteinase 2