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Open AccessArticle

Inhibition of Glioma Development by ASCL1-Mediated Direct Neuronal Reprogramming

Center for Brain Disorders Research, Capital Medical University; Center of Neural Injury and Repair, Beijing Institute for Brain Disorders, Beijing 100020, China
Institute of Neuroscience, Key Laboratory of Molecular Neurobiology of Ministry of Education and the Collaborative Innovation Center for Brain Science, Second Military Medical University, Shanghai 200433, China
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Cells 2019, 8(6), 571;
Received: 22 May 2019 / Revised: 8 June 2019 / Accepted: 10 June 2019 / Published: 11 June 2019
Direct conversion of non-neural cells into induced neurons holds great promise for brain repair. As the most common malignant tumor in the central nervous system, glioma is currently incurable due to its exponential growth and invasive behavior. Given that neurons are irreversible postmitotic cells, reprogramming glioma cells into terminally differentiated neuron-like cells represents a potential approach to inhibit brain tumor development. We here show that human glioma cells can be directly, rapidly and efficiently reprogrammed into terminally differentiated neuron-like cells by the single transcription factor ASCL1 (Achaete-scute complex-like 1, also known as MASH1). These induced cells exhibit typical neuron-like morphology and express multiple neuron-specific markers. Importantly, ASCL1-mediated neuronal reprogramming drives human glioma cells to exit the cell cycle and results in dramatic inhibition of proliferation, both in vitro and in vivo. Taken together, this proof-of-principle study demonstrates a potential strategy for impeding brain tumor development by ASCL1-induced direct neuronal reprogramming. View Full-Text
Keywords: ASCL1; reprogramming; glioma cells; neurons ASCL1; reprogramming; glioma cells; neurons
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Cheng, X.; Tan, Z.; Huang, X.; Yuan, Y.; Qin, S.; Gu, Y.; Wang, D.; He, C.; Su, Z. Inhibition of Glioma Development by ASCL1-Mediated Direct Neuronal Reprogramming. Cells 2019, 8, 571.

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