Runxin Wu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Runxin Wu has a total of 20 co-authors. Here are the top co-authors by number of shared publications:
- Allen Huff
Proteomics Platform, Office of Shared Research Facilities, Biological Sciences Division, University of Chicago, Chicago, IL 60637, USA
1 shared publication - Anshika Goenka
Northwestern University , Chicago , USA
1 shared publication - Bo Hu
The Ken & Ruth Davee Department of Neurology, The Lou and Jean Malnati Brain Tumor Institute, The Robert H. Lurie Comprehensive Cancer Center, Simpson Querrey Institute for Epigenetics, Northwestern University Feinberg School of Medicine , Chicago, Illinois
1 shared publication - Chang Zeng
Department of Preventive Medicine, The Robert H. Lurie Comprehensive Cancer Center, Simpson Querrey Institute for Epigenetics, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA
1 shared publication Christopher G. Hubert
Department of Biochemistry, School of Medicine, Case Western Reserved University, Cleveland, Ohio, USA
1 shared publication- Craig Horbinski
Department of Neurological Surgery, Northwestern University Feinberg School of Medicine, Chicago, USA
1 shared publication
Latest Publications
- Open Access
- 25 April 2024
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 134 (11)
RNA splicing analysis deciphers developmental hierarchies and reveals therapeutic targets in adult glioma
Widespread alterations in RNA alternative splicing (AS) have been identified in adult gliomas. However, their regulatory mechanism, biological significance, and therapeutic potential remain largely elusive. Here, using a computational approach with both bulk and single-cell RNA-Seq, we uncover a prognostic AS signature linked with neural developmental hierarchies. Using advanced iPSC glioma models driven by glioma driver mutations, we show that this AS signature could be enhanced by EGFRvIII and inhibited by in situ IDH1 mutation. Functional validations of 2 isoform switching events in CERS5 and MPZL1 show regulations of sphingolipid metabolism and SHP2 signaling, respectively. Analysis of upstream RNA binding proteins reveals PTBP1 as a key regulator of the AS signature where targeting of PTBP1 suppresses tumor growth and promotes the expression of a neuron marker TUJ1 in glioma stem-like cells. Overall, our data highlights the role of AS in affecting glioma malignancy and heterogeneity and its potential as a therapeutic vulnerability for treating adult gliomas.
- 25 April 2024
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 134 (11)
Open AccessRNA splicing analysis deciphers developmental hierarchies and reveals therapeutic targets in adult glioma
Widespread alterations in RNA alternative splicing (AS) have been identified in adult gliomas. However, their regulatory mechanism, biological significance, and therapeutic potential remain largely elusive. Here, using a computational approach with both bulk and single-cell RNA-Seq, we uncover a prognostic AS signature linked with neural developmental hierarchies. Using advanced iPSC glioma models driven by glioma driver mutations, we show that this AS signature could be enhanced by EGFRvIII and inhibited by in situ IDH1 mutation. Functional validations of 2 isoform switching events in CERS5 and MPZL1 show regulations of sphingolipid metabolism and SHP2 signaling, respectively. Analysis of upstream RNA binding proteins reveals PTBP1 as a key regulator of the AS signature where targeting of PTBP1 suppresses tumor growth and promotes the expression of a neuron marker TUJ1 in glioma stem-like cells. Overall, our data highlights the role of AS in affecting glioma malignancy and heterogeneity and its potential as a therapeutic vulnerability for treating adult gliomas.