TLR9 is critical for glioma stem cell maintenance and targeting.

نویسندگان

  • Andreas Herrmann
  • Gregory Cherryholmes
  • Anne Schroeder
  • Jillian Phallen
  • Darya Alizadeh
  • Hong Xin
  • Tianyi Wang
  • Heehyoung Lee
  • Christoph Lahtz
  • Piotr Swiderski
  • Brian Armstrong
  • Claudia Kowolik
  • Gary L Gallia
  • Michael Lim
  • Christine Brown
  • Behnam Badie
  • Stephen Forman
  • Marcin Kortylewski
  • Richard Jove
  • Hua Yu
چکیده

Understanding supports for cancer stem-like cells in malignant glioma may suggest therapeutic strategies for their elimination. Here, we show that the Toll-like receptor TLR9 is elevated in glioma stem-like cells (GSC) in which it contributes to glioma growth. TLR9 overexpression is regulated by STAT3, which is required for GSC maintenance. Stimulation of TLR9 with a CpG ligand (CpG ODN) promoted GSC growth, whereas silencing TLR9 expression abrogated GSC development. CpG-ODN treatment induced Frizzled4-dependent activation of JAK2, thereby activating STAT3. Targeted delivery of siRNA into GSC was achieved via TLR9 using CpG-siRNA conjugates. Through local or systemic treatment, administration of CpG-Stat3 siRNA to silence STAT3 in vivo reduced GSC along with glioma growth. Our findings identify TLR9 as a functional marker for GSC and a target for the delivery of efficacious therapeutics for glioma treatment. Cancer Res; 74(18); 5218-28. ©2014 AACR.

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عنوان ژورنال:
  • Cancer research

دوره 74 18  شماره 

صفحات  -

تاریخ انتشار 2014