| Literature DB >> 35994220 |
Cheng-Chen Zhang1, Ting Wu1, Li Guan1, Yu-Jue Wang1, Rui-Qin Yao1, Dian-Shuai Gao1, Feng Li2.
Abstract
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.Entities:
Keywords: Apoptosis; BP-1-102; Glioma; Invasion; Proliferation; STAT3
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Year: 2022 PMID: 35994220 DOI: 10.1007/s12013-022-01088-y
Source DB: PubMed Journal: Cell Biochem Biophys ISSN: 1085-9195 Impact factor: 2.989