双酚 S (BPS) 是双酚 A (BPA) 的替代品，具有与 BPA 类似的增殖作用。 BPS 是与癌症进展相关的代表性内分泌干扰物。然而，BPS 诱导的胶质母细胞瘤进展的机制尚不完全清楚。为了研究 BPS 对胶质母细胞瘤的影响，将 U-87 MG 癌细胞系暴露于 BPS。该研究重点分析 U-87 MG 细胞的增殖和迁移。此外，还检查了 zeste 同源物 2 (EZH2) 增强子介导的磷酸肌醇 3-激酶 (PI3K)/蛋白激酶 B (AKT)/雷帕霉素哺乳动物靶标 (mTOR) 通路的参与情况。采用药理学方法抑制EZH2活性并观察其对BPS诱导的变化的影响。结果表明，0.1μM浓度的BPS促进U-87 MG细胞的增殖和迁移。这些变化似乎与 EZH2 介导的 PI3K/AKT/mTOR 通路的激活有关。此外，使用药理学方法抑制 EZH2 活性可以恢复 BPS 介导的增殖和迁移诱导。总之，本研究结果表明 BPS 通过 EZH2 上调诱导胶质母细胞瘤进展。因此，针对 EZH2 介导的 PI3K/AKT/mTOR 通路可被视为治疗胶质母细胞瘤的潜在治疗策略。版权所有 © 2024 作者。由 Elsevier B.V. 出版。保留所有权利。

Bisphenol S (BPS), an alternative to bisphenol A (BPA), exerts proliferative effects similar to those of BPA. BPS is a representative endocrine disruptor associated with cancer progression. However, the mechanisms underlying BPS-induced glioblastoma progression are not fully understood. To investigate the effects of BPS on glioblastoma, U-87 MG cancer cell lines were exposed to BPS. The study focused on analyzing the proliferation and migration of U-87 MG cells. Furthermore, the involvement of the enhancer of the zeste homolog 2 (EZH2)-mediated phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of the rapamycin (mTOR) pathway was examined. Pharmacological approaches were employed to inhibit EZH2 activity and observe its effects on BPS-induced changes. The results indicated that BPS promoted the proliferation and migration of U-87 MG cells at a concentration of 0.1µM. These changes appeared to be linked to the activation of the EZH2-mediated PI3K/AKT/mTOR pathway. Moreover, inhibiting EZH2 activity using pharmacological approaches restored the BPS-mediated induction of proliferation and migration. In conclusion, the results of this study indicated that BPS induces glioblastoma progression through EZH2 upregulation. Therefore, targeting the EZH2-mediated PI3K/AKT/mTOR pathway could be considered a potential therapeutic strategy for the treatment of glioblastoma.Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.