HMMR maintains the stemness and tumorigenicity of glioblastoma stem-like cells.

Abstract	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, HMMR silencing suppresses GSC-derived tumor growth and extends the survival of mice bearing GSC xenografts. Conversely, HMMR overexpression promotes GSC self-renewal 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.
Authors	Jessica Tilghman, Hao Wu, Yingying Sang, Xiaohai Shi, Hugo Guerrero-Cazares, Alfredo Quinones-Hinojosa, Charles G Eberhart, John Laterra, Mingyao Ying
Journal	Cancer research (Cancer Res) Vol. 74 Issue 11 Pg. 3168-79 (Jun 01 2014) ISSN: 1538-7445 [Electronic] United States
PMID	24710409 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Copyright	©2014 American Association for Cancer Research.
Chemical References	Extracellular Matrix Proteins Hyaluronan Receptors hyaluronan-mediated motility receptor
Topics	Animals Carcinogenesis (genetics, metabolism, pathology) Cell Growth Processes (physiology) Cell Line, Tumor Extracellular Matrix Proteins (genetics, metabolism) Glioblastoma (genetics, metabolism, pathology) Humans Hyaluronan Receptors (genetics, metabolism) Mice Mice, SCID Neoplastic Stem Cells (metabolism, pathology)

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