Stanniocalcin-1 augments stem-like traits of glioblastoma cells through binding and activating NOTCH1

Cancer Lett. 2018 Mar 1:416:66-74. doi: 10.1016/j.canlet.2017.11.033. Epub 2017 Nov 28.

Abstract

Glioblastoma (GBM) is a fatal tumor and comprises heterogeneous cells in which a subpopulation with stem cell-like properties is included. Cancer cells with stem cell-like properties account for tumor initiation, drug resistance and recurrence. To identify and characterize specific factors in regulating stem-like traits is critical for GBM therapeutic. Here, we showed that Stanniocalcin-1 (STC1), a secretory glycoprotein, functions as a novel stimulator for stem-like traits of GBM cells. We found STC1 was prominently expressed in glioma spheres which are mainly comprised of glioma stem-like cells. The stem-like traits of GBM cells, as determined by the expression of stem cell markers, tumor-sphere formation efficiency and colony-forming ability, were enhanced by STC1 overexpression and inhibited by STC1 knockdown. Furthermore, introduction of STC1 enhanced tumorigenesis in vivo while knockdown of STC1 showed reverse effect. Finally, we demonstrated that STC1 interacted with the extracellular domain of NOTCH1 to activate NOTCH1-SOX2 signaling pathway, by which STC1 augmented the stem-like traits of GBM cells. Taken together, our data herein indicate that STC1 is a novel non-canonical NOTCH ligand and acts as a crucial regulator of stemness in GBM.

Keywords: Glioblastoma; NOTCH1; SOX2; Stanniocalcin-1; Stemness.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain Neoplasms / genetics*
  • Brain Neoplasms / metabolism
  • Brain Neoplasms / pathology
  • Cell Line, Tumor
  • Gene Expression Regulation, Neoplastic*
  • Glioblastoma / genetics*
  • Glioblastoma / metabolism
  • Glioblastoma / pathology
  • Glycoproteins / genetics*
  • Glycoproteins / metabolism
  • HEK293 Cells
  • Humans
  • Kaplan-Meier Estimate
  • Male
  • Mice, Inbred BALB C
  • Mice, Nude
  • Neoplastic Stem Cells / metabolism*
  • Protein Binding
  • RNA Interference
  • Receptor, Notch1 / genetics*
  • Receptor, Notch1 / metabolism
  • Transplantation, Heterologous

Substances

  • Glycoproteins
  • NOTCH1 protein, human
  • Receptor, Notch1
  • teleocalcin