Malignant glioma, especially glioblastoma (GBM), has historically been associated with a low survival rate. The hyperactivation of STAT3 played a key role in GBM initiation and resistance to therapy; thus, there is an urgent requirement for novel STAT3 inhibitors. BP-1-102 was recently reported as a biochemical inhibitor of STAT3, but its roles and mechanism in biological behavior of glioma cells were still unclear. In this study, the effects of BP-1-102 on proliferation, apoptosis, invasion and neurosphere formation of glioma cell were investigated. Our results indicated that BP-1-102 inhibited the proliferation of U251 and A172 cells, and their IC50 values were 10.51 and 8.534 μM, respectively. Furthermore, BP-1-102 inhibited the invasion and migration abilities of U251 and A172 cells by decreasing the expression of matrix metallopeptidase 9, and induced glioma cell apoptosis by decreasing the expression of B-cell lymphoma-2. BP-1-102 also inhibited the formation of neurosphere. Mechanically, BP-1-102 reduced the phosphorylation of STAT3 and the p-STAT3’s nuclear translocation in glioma cells. Thus, this study herein provided a potential drug for glioma therapy.

恶性胶质瘤，尤其是胶质母细胞瘤 (GBM)，历来与低存活率有关。STAT3 的过度激活在 GBM 的启动和治疗抵抗中起关键作用；因此，迫切需要新型 STAT3 抑制剂。BP-1-102最近被报道为STAT3的生化抑制剂，但其在胶质瘤细胞生物学行为中的作用和机制仍不清楚。本研究探讨了BP-1-102对胶质瘤细胞增殖、凋亡、侵袭和神经球形成的影响。我们的结果表明，BP-1-102 抑制 U251 和 A172 细胞的增殖，其 IC50 值分别为 10.51 和 8.534 μM。此外，BP-1-102 通过降低基质金属肽酶 9 的表达来抑制 U251 和 A172 细胞的侵袭和迁移能力，并通过降低 B 细胞淋巴瘤 2 的表达诱导胶质瘤细胞凋亡。BP-1-102 还抑制神经球的形成。机械地，BP-1-102 减少了胶质瘤细胞中 STAT3 的磷酸化和 p-STAT3 的核转位。因此，本研究提供了一种潜在的神经胶质瘤治疗药物。