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Title: IGFBP2 promotes glioma tumor stem cell expansion and survival

Abstract

IGFBP2 is overexpressed in the most common brain tumor, glioblastoma (GBM), and its expression is inversely correlated to GBM patient survival. Previous reports have demonstrated a role for IGFBP2 in glioma cell invasion and astrocytoma development. However, the function of IGFBP2 in the restricted, self-renewing, and tumorigenic GBM cell population comprised of tumor-initiating stem cells has yet to be determined. Herein we demonstrate that IGFBP2 is overexpressed within the stem cell compartment of GBMs and is integral for the clonal expansion and proliferative properties of glioma stem cells (GSCs). In addition, IGFBP2 inhibition reduced Akt-dependent GSC genotoxic and drug resistance. These results suggest that IGFBP2 is a selective malignant factor that may contribute significantly to GBM pathogenesis by enriching for GSCs and mediating their survival. Given the current dearth of selective molecular targets against GSCs, we anticipate our results to be of high therapeutic relevance in combating the rapid and lethal course of GBM.

Authors:
 [1];  [2];  [3];  [1]
  1. College of Medicine, The University of Arizona (United States)
  2. The McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine (United States)
  3. Department of Radiation Oncology, The University of Arizona (United States)
Publication Date:
OSTI Identifier:
22202668
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 397; Journal Issue: 2; Other Information: Copyright (c) 2010 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; BRAIN; DRUGS; GLIOMAS; INHIBITION; PATHOGENESIS; PATIENTS; STEM CELLS

Citation Formats

Hsieh, David, Hsieh, Antony, Stea, Baldassarre, and Ellsworth, Ron. IGFBP2 promotes glioma tumor stem cell expansion and survival. United States: N. p., 2010. Web. doi:10.1016/J.BBRC.2010.05.145.
Hsieh, David, Hsieh, Antony, Stea, Baldassarre, & Ellsworth, Ron. IGFBP2 promotes glioma tumor stem cell expansion and survival. United States. https://doi.org/10.1016/J.BBRC.2010.05.145
Hsieh, David, Hsieh, Antony, Stea, Baldassarre, and Ellsworth, Ron. 2010. "IGFBP2 promotes glioma tumor stem cell expansion and survival". United States. https://doi.org/10.1016/J.BBRC.2010.05.145.
@article{osti_22202668,
title = {IGFBP2 promotes glioma tumor stem cell expansion and survival},
author = {Hsieh, David and Hsieh, Antony and Stea, Baldassarre and Ellsworth, Ron},
abstractNote = {IGFBP2 is overexpressed in the most common brain tumor, glioblastoma (GBM), and its expression is inversely correlated to GBM patient survival. Previous reports have demonstrated a role for IGFBP2 in glioma cell invasion and astrocytoma development. However, the function of IGFBP2 in the restricted, self-renewing, and tumorigenic GBM cell population comprised of tumor-initiating stem cells has yet to be determined. Herein we demonstrate that IGFBP2 is overexpressed within the stem cell compartment of GBMs and is integral for the clonal expansion and proliferative properties of glioma stem cells (GSCs). In addition, IGFBP2 inhibition reduced Akt-dependent GSC genotoxic and drug resistance. These results suggest that IGFBP2 is a selective malignant factor that may contribute significantly to GBM pathogenesis by enriching for GSCs and mediating their survival. Given the current dearth of selective molecular targets against GSCs, we anticipate our results to be of high therapeutic relevance in combating the rapid and lethal course of GBM.},
doi = {10.1016/J.BBRC.2010.05.145},
url = {https://www.osti.gov/biblio/22202668}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 2,
volume = 397,
place = {United States},
year = {Fri Jun 25 00:00:00 EDT 2010},
month = {Fri Jun 25 00:00:00 EDT 2010}
}