Research Papers:

Emx2 as a novel tool to suppress glioblastoma

Carmen Falcone _, Antonio Daga, Giampiero Leanza and Antonello Mallamaci

PDF  |  HTML  |  Supplementary Files  |  How to cite  |  Order a Reprint

Oncotarget. 2016; 7:41005-41016. https://doi.org/10.18632/oncotarget.9322

Metrics: PDF 1589 views  |   HTML 1998 views  |   ?  


Carmen Falcone1, Antonio Daga2, Giampiero Leanza3, Antonello Mallamaci1

1Department of Neuroscience, SISSA, 34136 Trieste, Italy

2DIPOE, IRCCS AOU San Martino IST, 16132 Genoa, Italy

3Department of Life Sciences, University of Trieste, 34127 Trieste, Italy

Correspondence to:

Antonello Mallamaci, email: amallama@sissa.it

Keywords: Emx2, glioblastoma, gene therapy, EGFR, SOX2

Received: February 28, 2016    Accepted: April 26, 2016    Published: May 13, 2016


Glioblastoma is a devastating CNS tumour for which no cure is presently available. We wondered if manipulation of Emx2, which normally antagonizes cortico-cerebral astrogenesis by inhibiting proliferation of astrocyte progenitors, may be employed to counteract it. We found that Emx2 overexpression induced the collapse of seven out of seven in vitro tested glioblastoma cell lines. Moreover, it suppressed four out of four of these lines in vivo. As proven by dedicated rescue assays, the antioncogenic activity of Emx2 originated from its impact on at least six metabolic nodes, which accounts for the robustness of its effect. Finally, in two out of two tested lines, the tumor culture collapse was also achieved when Emx2 was driven by a neural stem cell-specific promoter, likely active within tumor-initiating cells. All that points to Emx2 as a novel, promising tool for therapy of glioblastoma and prevention of its recurrencies.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 9322