The tumor susceptibility gene 101 (TSG101) has been reported to play important roles in the development and progression of several human cancers, such as pancreatic cancer, prostate cancer, and hepatocellular carcinoma. However, its potential roles and underlined mechanisms in human glioma are still needed to be further clarified. This study was designed to assess the expression of TSG101 in glioma patients and its effects on glioma cell proliferation, migration, and invasion. Publicly available data revealed that TSG101 mRNA was significantly upregulated in glioma tissues, and high levels of TSG101 were associated with poor prognosis in glioma patients. Western blot and immunohistochemistry experiments further showed that the expression level of TSG101 protein was significantly upregulated in glioma patients, especially in the patients with high-grade glioma. The functional studies showed that knockdown of TSG101 suppressed the proliferation, migration, and invasion of glioma cells, while overexpression of TSG101 facilitated them. Mechanistic studies indicated that the proliferation, migration, and invasion induced by TSG101 in human glioma were related to AKT/GSK3β/β-catenin and RhoC/Cofilin signaling pathways. In conclusion, the above results suggest that the expression of TSG101 is elevated in glioma patients, which accelerates the proliferation, migration, and invasion of glioma cells by regulating the AKT/GSK3β/β-catenin and RhoC/Cofilin pathways.

据报道，肿瘤易感基因 101 (TSG101) 在多种人类癌症的发展和进展中发挥重要作用，例如胰腺癌、前列腺癌和肝细胞癌。然而，其在人类胶质瘤中的潜在作用和突出机制仍有待进一步阐明。本研究旨在评估 TSG101 在胶质瘤患者中的表达及其对胶质瘤细胞增殖、迁移和侵袭的影响。公开数据显示，TSG101 mRNA 在胶质瘤组织中显着上调，高水平的 TSG101 与胶质瘤患者的不良预后相关。Western印迹和免疫组化实验进一步表明，TSG101蛋白在胶质瘤患者中的表达水平显着上调，尤其是高级别胶质瘤患者。功能研究表明，TSG101 的敲低抑制了胶质瘤细胞的增殖、迁移和侵袭，而 TSG101 的过表达促进了它们。机制研究表明，TSG101在人脑胶质瘤中诱导的增殖、迁移和侵袭与AKT/GSK3β/β-catenin和RhoC/Cofilin信号通路有关。综上所述，上述结果提示TSG101在胶质瘤患者中表达升高，通过调节AKT/GSK3β/β-catenin和RhoC/Cofilin通路加速胶质瘤细胞的增殖、迁移和侵袭。机制研究表明，TSG101在人脑胶质瘤中诱导的增殖、迁移和侵袭与AKT/GSK3β/β-catenin和RhoC/Cofilin信号通路有关。综上所述，上述结果提示TSG101在胶质瘤患者中表达升高，通过调节AKT/GSK3β/β-catenin和RhoC/Cofilin通路加速胶质瘤细胞的增殖、迁移和侵袭。机制研究表明，TSG101在人脑胶质瘤中诱导的增殖、迁移和侵袭与AKT/GSK3β/β-catenin和RhoC/Cofilin信号通路有关。综上所述，上述结果提示TSG101在胶质瘤患者中表达升高，通过调节AKT/GSK3β/β-catenin和RhoC/Cofilin通路加速胶质瘤细胞的增殖、迁移和侵袭。