Selective cytotoxicity of solamargine via oxidative stress and caspase-independent mechanisms in human glioblastoma cells

茄碱通过氧化应激和非caspase依赖性机制对人胶质母细胞瘤细胞产生选择性细胞毒性

阅读:1

Abstract

IDH-wild-type glioblastoma (IDH-wildtype GB) is an aggressive and genetically heterogeneous tumor characterized by intrinsic resistance to radiotherapy and chemotherapy, while surgical resection remains inherently limited by its diffuse infiltrative growth, leading to poor clinical outcomes. Natural products such as solamargine (SM), a steroidal glycoalkaloid with cytotoxic and antitumor properties, have emerged as potential adjuvant strategies. Here, we investigated the effects of SM on proliferation, clonogenic survival, morphology and migration of IDH-wildtype GB cell lines (U-87MG, U-251MG and T98-G) and non-tumoral astrocytes under normoxic and hypoxic conditions, as well as its interaction with temozolomide (TMZ). Under normoxia, SM reduced cell viability in a dose- and time-dependent manner, with IC₅₀ values between 5.04 and 9.53 μM and showed enhanced cytotoxicity under hypoxia. TMZ alone displayed modest activity, and its combination with SM produced predominantly antagonistic effects. Clonogenic assays confirmed the antiproliferative potential of SM, with significant inhibition of colony formation at 2.5 μM. SM induced marked morphological alterations but did not significantly impair migration in wound-healing assays. In U-87MG cells, SM triggered G₂/M cell-cycle arrest, increased intracellular reactive oxygen species generation, and elevated γH2AX protein expression, indicating oxidative stress-associated DNA damage. However, cleaved caspase-3 and p53 were not detected, suggesting a predominantly non-apoptotic mode of cell death. Together, these findings support SM as a promising candidate for IDH-wildtype GB therapy and underscore the need for further studies to clarify its mechanisms of action and optimize its therapeutic use.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。