Customer Publication

m5C modification of LINC00324 promotes angiogenesis in glioma through CBX3/VEGFR2 pathway

Authors: A. Pan et al.

Journal: International Journal of Biological Macromolecules (2023)

Research Areas: Cancer Research

Cell Lines: GECs, hCMEC/D3, SVG p12, U-251MG (glioblastoma endothelial cells, human brain microvascular endothelial cell line, Human astrocyte, Human glioblastoma cell line)

Summary: 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. HoloMonitor M4 was used to study the migration of cells with NSUN2 or LINC00324 knockdown with single cell tracking assay.

Keywords: HoloMonitor M4, single cell tracking assay, NSUN2 5-methylcytosine, LINC00324, CBX3, glioma, angiogenesis

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