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.

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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