Abstract：
BACKGROUND: Protein tyrosine phosphatase non-receptor type 7 (PTPN7) is a signaling molecule that regulates a multitude of cellular processes, spanning cell proliferation, cellular differentiation, the mitotic cycle, and oncogenic metamorphosis. However, the characteristic of PTPN7 in the glioma microenvironment has yet to be elucidated.
METHODS: The prognostic value, genomic features, immune characteristics, chemotherapy prediction, and immunotherapy prediction of PTPN7 were systematically explored at the bulk sequencing level. The cell evolution trajectory, cell communication pattern, and cell metabolic activity related to PTPN7 were systematically explored at the single-cell sequencing level. HMC3 and M0 cells were cocultured with U251 and T98G cells, and flow cytometry was carried out to investigate the polarization of HMC3 and M0. Transwell assay and CCK-8 assay were performed to explore the migration and proliferation activity of U251 and T98G.
RESULTS: The expression level of PTPN7 is significantly elevated in glioma and indicates malignant features. PTPN7 expression predicts worse prognosis of glioma patients. PTPN7 is associated with genome alteration and immune infiltration. Besides, PTPN7 plays a crucial role in modulating metabolic and immunogenic processes, particularly by influencing the activity of microglia and macrophages through multiple signaling pathways involved in cellular communication. Specifically, PTPN7 actively mediates inflammation-resolving-polarization of macrophages and microglia and protects glioma from immune attack. PTPN7 could also predict the response of immunotherapy.
CONCLUSIONS: PTPN7 is critically involved in inflammation-resolving-polarization mediated by macrophage and microglia and promotes the immune escape of glioma cells.
METHODS: The prognostic value, genomic features, immune characteristics, chemotherapy prediction, and immunotherapy prediction of PTPN7 were systematically explored at the bulk sequencing level. The cell evolution trajectory, cell communication pattern, and cell metabolic activity related to PTPN7 were systematically explored at the single-cell sequencing level. HMC3 and M0 cells were cocultured with U251 and T98G cells, and flow cytometry was carried out to investigate the polarization of HMC3 and M0. Transwell assay and CCK-8 assay were performed to explore the migration and proliferation activity of U251 and T98G.
RESULTS: The expression level of PTPN7 is significantly elevated in glioma and indicates malignant features. PTPN7 expression predicts worse prognosis of glioma patients. PTPN7 is associated with genome alteration and immune infiltration. Besides, PTPN7 plays a crucial role in modulating metabolic and immunogenic processes, particularly by influencing the activity of microglia and macrophages through multiple signaling pathways involved in cellular communication. Specifically, PTPN7 actively mediates inflammation-resolving-polarization of macrophages and microglia and protects glioma from immune attack. PTPN7 could also predict the response of immunotherapy.
CONCLUSIONS: PTPN7 is critically involved in inflammation-resolving-polarization mediated by macrophage and microglia and promotes the immune escape of glioma cells.
摘要：
背景：蛋白酪氨酸磷酸酶非受体7型（PTPN7）是调节多种细胞过程的信号分子，跨越细胞增殖，细胞分化，有丝分裂周期，和致癌变态。然而,PTPN7在神经胶质瘤微环境中的特征尚未阐明。
方法：预后价值，基因组特征，免疫特性，化疗预测，在批量测序水平上系统地探索了PTPN7的免疫治疗预测。细胞进化轨迹，细胞通信模式，在单细胞测序水平上系统地探讨了与PTPN7相关的细胞代谢活性。HMC3和M0细胞与U251和T98G细胞共培养，并进行流式细胞术研究HMC3和M0的极化。进行Transwell测定和CCK-8测定以探讨U251和T98G的迁移和增殖活性。
结果：PTPN7的表达水平在神经胶质瘤中显著升高，并显示恶性特征。PTPN7表达预测胶质瘤患者预后较差。PTPN7与基因组改变和免疫浸润有关。此外,PTPN7在调节代谢和免疫原性过程中起着至关重要的作用，特别是通过参与细胞通讯的多个信号通路影响小胶质细胞和巨噬细胞的活性。具体来说,PTPN7积极介导巨噬细胞和小胶质细胞的炎症解决极化并保护神经胶质瘤免受免疫攻击。PTPN7还可以预测免疫治疗的反应。
结论：PTPN7与巨噬细胞和小胶质细胞介导的炎症消退极化密切相关，并促进神经胶质瘤细胞的免疫逃逸。
方法：预后价值，基因组特征，免疫特性，化疗预测，在批量测序水平上系统地探索了PTPN7的免疫治疗预测。细胞进化轨迹，细胞通信模式，在单细胞测序水平上系统地探讨了与PTPN7相关的细胞代谢活性。HMC3和M0细胞与U251和T98G细胞共培养，并进行流式细胞术研究HMC3和M0的极化。进行Transwell测定和CCK-8测定以探讨U251和T98G的迁移和增殖活性。
结果：PTPN7的表达水平在神经胶质瘤中显著升高，并显示恶性特征。PTPN7表达预测胶质瘤患者预后较差。PTPN7与基因组改变和免疫浸润有关。此外,PTPN7在调节代谢和免疫原性过程中起着至关重要的作用，特别是通过参与细胞通讯的多个信号通路影响小胶质细胞和巨噬细胞的活性。具体来说,PTPN7积极介导巨噬细胞和小胶质细胞的炎症解决极化并保护神经胶质瘤免受免疫攻击。PTPN7还可以预测免疫治疗的反应。
结论：PTPN7与巨噬细胞和小胶质细胞介导的炎症消退极化密切相关，并促进神经胶质瘤细胞的免疫逃逸。
