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

Jessica Tilghman, Hao Wu, Yingying Sang, Xiaohai Shi, Hugo Guerrero-Cazares, Alfredo Quinones-Hinojosa, Charles G. Eberhart, John Laterra, Mingyao Ying

Research output: Contribution to journalArticlepeer-review

66 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)3168-3179
Number of pages12
JournalCancer research
Issue number11
StatePublished - Jun 1 2014

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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