TY - JOUR
T1 - HMMR maintains the stemness and tumorigenicity of glioblastoma stem-like cells
AU - Tilghman, Jessica
AU - Wu, Hao
AU - Sang, Yingying
AU - Shi, Xiaohai
AU - Guerrero-Cazares, Hugo
AU - Quinones-Hinojosa, Alfredo
AU - Eberhart, Charles G.
AU - Laterra, John
AU - Ying, Mingyao
PY - 2014/6/1
Y1 - 2014/6/1
N2 - Glioblastoma (GBM) stem cells (GSC) are a subpopulation of tumor cells that display stem-like characteristics (stemness) and play unique roles in tumor propagation, therapeutic resistance, and tumor recurrence. Therapeutic targets in GSCs are a focus of increasing interest to improve GBM therapy. Here we report that the hyaluronan-mediated motility receptor (HMMR) is highly expressed in GBM tumors, where it supports the self-renewal and tumorigenic potential of GSCs. HMMR silencing impairs GSC self-renewal and inhibits the expression of GSC markers and regulators. Furthermore,HMMRsilencing suppresses GSC-derived tumor growth and extends the survival of mice bearing GSC xenografts. Conversely, HMMR overexpression promotes GSC selfrenewal and intracranial tumor propagation. In human GBM tumor specimens, HMMR expression is correlated positively with the expression of stemness-associated markers and regulators. Our findings identify HMMR as a candidate therapeutic target to GSCs as a GBM treatment strategy.
AB - Glioblastoma (GBM) stem cells (GSC) are a subpopulation of tumor cells that display stem-like characteristics (stemness) and play unique roles in tumor propagation, therapeutic resistance, and tumor recurrence. Therapeutic targets in GSCs are a focus of increasing interest to improve GBM therapy. Here we report that the hyaluronan-mediated motility receptor (HMMR) is highly expressed in GBM tumors, where it supports the self-renewal and tumorigenic potential of GSCs. HMMR silencing impairs GSC self-renewal and inhibits the expression of GSC markers and regulators. Furthermore,HMMRsilencing suppresses GSC-derived tumor growth and extends the survival of mice bearing GSC xenografts. Conversely, HMMR overexpression promotes GSC selfrenewal and intracranial tumor propagation. In human GBM tumor specimens, HMMR expression is correlated positively with the expression of stemness-associated markers and regulators. Our findings identify HMMR as a candidate therapeutic target to GSCs as a GBM treatment strategy.
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UR - http://www.scopus.com/inward/citedby.url?scp=84902186974&partnerID=8YFLogxK
U2 - 10.1158/0008-5472.CAN-13-2103
DO - 10.1158/0008-5472.CAN-13-2103
M3 - Article
C2 - 24710409
AN - SCOPUS:84902186974
SN - 0008-5472
VL - 74
SP - 3168
EP - 3179
JO - Cancer research
JF - Cancer research
IS - 11
ER -