The transcriptional modulator HMGA2 promotes stemness and tumorigenicity in glioblastoma

Harpreet Kaur, Sabeen Zulfiqar Ali, Lauren Huey, Marianne Hütt-Cabezas, Isabella Taylor, Xing gang Mao, Melanie Weingart, Qian Chu, Fausto J. Rodriguez, Charles G. Eberhart, Eric H. Raabe

Research output: Contribution to journalArticlepeer-review

34 Scopus citations


Glioblastoma (GBM) contains a population of stem-like cells that promote tumor invasion and resistance to therapy. Identifying and targeting stem cell factors in GBM may lead to the development of more effective therapies. High Mobility Group AT-hook 2 (HMGA2) is a transcriptional modulator that mediates motility and self-renewal in normal and cancer stem cells. We identified increased expression of HMGA2 in the majority of primary human GBM tumors and cell lines compared to normal brain. Additionally, HMGA2 expression was increased in CD133+ GBM neurosphere cells compared to CD133- cells. Targeting HMGA2 with lentiviral short hairpin RNA (shRNA) led to decreased GBM stemness, invasion, and tumorigenicity. Ectopic expression of HMGA2 in GBM cell lines promoted stemness, invasion, and tumorigenicity. Our data suggests that targeting HMGA2 in GBM may be therapeutically beneficial.

Original languageEnglish (US)
Pages (from-to)55-64
Number of pages10
JournalCancer Letters
Issue number1
StatePublished - Jul 10 2016


  • Clonogenicity
  • GSC
  • Glioma
  • HMGI-C
  • Motility

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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