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Updated: Jul 9, 2025

Author Spotlight: Investigating Angiogenesis and Vessel Permeability Through a Modified Matrix Gel Plug Assay
Published on: June 30, 2023
m5C modification of LINC00324 promotes angiogenesis in glioma through CBX3/VEGFR2 pathway
Aini Pan1, Yixue Xue1, Xuelei Ruan1
1Department of Neurobiology, School of Life Sciences, China Medical University, Shenyang 110122, China; Key Laboratory of Neuro-oncology in Liaoning Province, Shenyang 110004, China.
Abstract:
Angiogenesis plays a major role in tumor initiation, progression, and metastasis. This is why finding antiangiogenic targets is essential in the treatment of gliomas. In this study, NSUN2 and LINC00324 were significantly upregulated in conditionally cultured glioblastoma endothelial cells (GECs). Knockdown of NSUN2 or LINC00324 inhibits GECs angiogenesis. NSUN2 increased the stability of LINC00324 by m5C modification and upregulated LINC00324 expression. LINC00324 competes with the 3'UTR of CBX3 mRNA to bind to AUH protein, reducing the degradation of CBX3 mRNA. In addition, CBX3 directly binds to the promoter region of VEGFR2, enhances VEGFR2 transcription, and promotes GECs angiogenesis. These findings demonstrated NSUN2/LINC00324/CBX3 axis plays a crucial role in regulating glioma angiogenesis, which provides new strategies for glioma therapy.
Insights
This study identifies the NSUN2/LINC00324/CBX3 axis as a key regulator of glioma angiogenesis. Targeting this pathway offers novel therapeutic strategies for treating gliomas by inhibiting tumor blood vessel formation.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Angiogenesis is critical for glioma development, progression, and metastasis.
- Identifying effective antiangiogenic targets is essential for glioma treatment.
Purpose of the Study:
- To investigate the role of NSUN2 and LINC00324 in glioma angiogenesis.
- To elucidate the molecular mechanisms underlying their regulation of endothelial cell function.
Main Methods:
- Studied conditionally cultured glioblastoma endothelial cells (GECs).
- Utilized knockdown techniques for NSUN2 and LINC00324.
- Analyzed m5C modification, mRNA stability, protein binding, and gene transcription.
Main Results:
- NSUN2 and LINC00324 were upregulated in GECs and promoted angiogenesis.
- NSUN2 stabilized LINC00324 via m5C modification, increasing its expression.
- LINC00324 reduced CBX3 mRNA degradation, and CBX3 enhanced VEGFR2 transcription, promoting angiogenesis.
Conclusions:
- The NSUN2/LINC00324/CBX3 axis is a crucial regulator of glioma angiogenesis.
- This axis provides potential new therapeutic targets for glioma treatment.
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