Department of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei Province, China.
Department of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei Province, China; Department of Central Laboratory, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei Province, China.
Int Immunopharmacol. 2024 Dec 25;143(Pt 1):113314. doi: 10.1016/j.intimp.2024.113314. Epub 2024 Oct 11.
Gliomas are the most common malignant brain tumor in the central nervous system. They are characterized by high invasiveness and heterogeneity. In recent years, cancer-derived immunoglobulin G (Cancer-IgG) has received significant attention from researchers. Cancer-IgG, identified from tumors, can promote tumorigenesis and tumor progression. In this study, we explored the expression patterns of Cancer-IgG using available datasets and validated these patterns in our patient samples. Several loss-of-function and gain-of function assays were performed to investigate the roles of Cancer-IgG. Potential mechanisms underlying these roles were investigated using co-immunoprecipitation and RNA sequencing. Our result demonstrated that Cancer-IgG is expressed in gliomas. Furthermore, the expression of Cancer-IgG is associated with a poor prognosis and malignant molecular characterization. Functional assays confirmed that Cancer-IgG can promote glioma cells proliferation, migration, invasion, and resistant to apoptosis. The cGMP/PKG/VASP pathway is potentially involved in the effects of Cancer-IgG. Evidence from co-culture assay suggest that Cancer-IgG can induce M2 polarization of macrophages. In conclusion, Cancer-IgG can be identified in glioma cells and promotes the development of a malignant biological phenotype in vivo and in vitro. In glioma microenvironment, Cancer-IgG can induce M2 polarization of macrophages.
神经胶质瘤是中枢神经系统中最常见的恶性脑肿瘤。它们的特点是高侵袭性和异质性。近年来,源自肿瘤的免疫球蛋白 G(Cancer-IgG)引起了研究人员的广泛关注。从肿瘤中鉴定出的 Cancer-IgG 可以促进肿瘤发生和肿瘤进展。在这项研究中,我们使用现有数据集探索了 Cancer-IgG 的表达模式,并在我们的患者样本中验证了这些模式。进行了几种失活和获得功能的测定来研究 Cancer-IgG 的作用。使用共免疫沉淀和 RNA 测序研究了这些作用的潜在机制。我们的结果表明 Cancer-IgG 在神经胶质瘤中表达。此外,Cancer-IgG 的表达与预后不良和恶性分子特征有关。功能测定证实 Cancer-IgG 可以促进神经胶质瘤细胞的增殖、迁移、侵袭和抗凋亡。cGMP/PKG/VASP 途径可能参与了 Cancer-IgG 的作用。共培养实验的证据表明,Cancer-IgG 可以诱导巨噬细胞的 M2 极化。总之,Cancer-IgG 可以在神经胶质瘤细胞中被识别,并在体内和体外促进恶性生物学表型的发展。在神经胶质瘤微环境中,Cancer-IgG 可以诱导巨噬细胞的 M2 极化。