Commentary 10.1172/JCI128742

Deubiquitinating ALDH1A3 key to maintaining the culprit of aggressive brain cancer

Hiroaki Wakimoto

Department of Neurosurgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Address correspondence to: Hiroaki Wakimoto, CPZN-3800, 185 Cambridge Street, Boston, Massachusetts 02114, USA. Phone: 617.643.5987; Email: hwakimoto@mgh.harvard.edu.

Find articles by Wakimoto, H. in: JCI | PubMed | Google Scholar |

First published April 8, 2019 - More info

Published in Volume 129, Issue 5 on May 1, 2019
J Clin Invest. 2019;129(5):1833–1835. https://doi.org/10.1172/JCI128742.
© 2019 American Society for Clinical Investigation
First published April 8, 2019 - Version history

Cancer stem cells sustain propagation of the deadly primary brain cancer glioblastoma. Glioblastoma stem cells (GSCs) characterized by a mesenchymal phenotype are aggressive and resistant to therapies and represent a crucial therapeutic target. In this issue of the JCI, Chen et al. show that the intracellular levels of aldehyde dehydrogenase 1A3 (ALDH1A3), known as a functional marker of mesenchymal GSCs, are regulated posttranslationally by ubiquitin-specific protease 9X–mediated (USP9X-mediated) deubiquitination. Increased expression of USP9X stabilizes ALDH1A3, enabling GSCs to exhibit mesenchymal traits and the malignant phenotype. Thus, the USP9X-ALDH1A3 axis may offer a novel therapeutic target in glioblastoma.

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