ZHANG Huimin, LIAO Liting, HU Chunmiao, HU Xiangyu, GONG Weijuan, JIA Xiaoqin. Effects of glycosylphosphatidylinositol-anchored HDL-binding protein on glioma growth and macrophage infiltration[J]. Journal of Clinical Medicine in Practice, 2024, 28(19): 1-9. DOI: 10.7619/jcmp.20241428
Citation: ZHANG Huimin, LIAO Liting, HU Chunmiao, HU Xiangyu, GONG Weijuan, JIA Xiaoqin. Effects of glycosylphosphatidylinositol-anchored HDL-binding protein on glioma growth and macrophage infiltration[J]. Journal of Clinical Medicine in Practice, 2024, 28(19): 1-9. DOI: 10.7619/jcmp.20241428

Effects of glycosylphosphatidylinositol-anchored HDL-binding protein on glioma growth and macrophage infiltration

  • Objective To investigate the effects of glycosylphosphatidylinositol-anchored HDL-binding protein (GPIHBP1) on glioma growth and macrophage infiltration.
    Methods Initially, the expression of GPIHBP1 in glioma samples and macrophage infiltration were analyzed using TCGA database, and these bioinformatics results were validated in clinical tissue samples. A stable glioma cell line overexpressing GPIHBP1 was then established to further explore the effects of GPIHBP1 overexpression on glioma cell proliferation, apoptosis, migration, and invasion. Finally, the impact of GPIHBP1 overexpression on tumor growth and macrophage infiltration was verified through xenograft experiments.
    Results TCGA database analysis revealed that GPIHBP1 expression was higher in low-grade gliomas compared to normal tissues, while it was lower in high-grade gliomas. Additionally, the expression level of GPIHBP1 in low-grade gliomas was higher than in high-grade gliomas, which was confirmed by immunohistochemistry (IHC). Western blot analysis confirmed the successful construction of the GPIHBP1-overexpressing glioma cell line. CCK-8, flow cytometry, scratch and Transwell assays demonstrated that the proliferation, migration and invasion capabilities of the stable cell line were reduced compared to the control group. Xenograft experiments further showed that the tumor growth and macrophage infiltration were decreased in the stable cell line.
    Conclusion The differential expression of GPIHBP1 in different grades of gliomas may be associated with tumor progression. Overexpression of GPIHBP1 can inhibit glioma growth, possibly by influencing the tumor microenvironment and promoting the polarization of macrophages towards the antitumor M1 phenotype, thereby inhibiting glioma growth.
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