Jamali Abdul Wahab, Zhanzhan Zhang, Sun Boyu, Song Zihan, Mehmood Arshad, Liu Liqiang
Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
Contemp Oncol (Pozn). 2025;29(2):195-205. doi: 10.5114/wo.2025.150649. Epub 2025 May 12.
This study aimed to investigate the role of in the proliferation, invasion, and expression of U251 glioblastoma cells, using both and methodologies.
This study investigated the role of , an RNA demethylase, in regulating the proliferation, invasion, and ferroptotic sensitivity of U251 glioblastoma cells, with a focus on its interplay with , a transmembrane glycoprotein implicated in tumour progression and stress responses.
Using in vitro and in vivo models, we demonstrate that knockdown significantly inhibits U251 cell proliferation, invasion, and tumour growth, while its overexpression enhances these oncogenic properties. regulates expression, with overexpression that rescues the inhibitory effects of knockdown on cell viability and invasion. We uncover a novel link between and ferroptosis, i.e. that knockdown sensitises U251 cells to ferroptotic cell death through modulation of -mediated lipid peroxidation and iron metabolism pathways. studies reveal reduced tumour growth and Ki-67 expression in knockdown models with decreased levels in tumour tissues.
The results highlight as a critical regulator of glioblastoma progression and ferroptotic sensitivity, with acting as a key downstream effector. Our findings provide new insights into the molecular mechanisms that drive glioblastoma aggressiveness and propose and as promising therapeutic targets for combating this lethal disease.
本研究旨在使用[具体方法1]和[具体方法2]方法，研究[物质名称]在U251胶质母细胞瘤细胞增殖、侵袭及[相关蛋白名称]表达中的作用。
本研究调查了一种RNA去甲基化酶[物质名称]在调节U251胶质母细胞瘤细胞增殖、侵袭和铁死亡敏感性中的作用，重点关注其与一种参与肿瘤进展和应激反应的跨膜糖蛋白[相关蛋白名称]的相互作用。
使用体外和体内模型，我们证明[物质名称]敲低显著抑制U251细胞增殖、侵袭和肿瘤生长，而其过表达增强了这些致癌特性。[物质名称]调节[相关蛋白名称]表达，[相关蛋白名称]过表达可挽救[物质名称]敲低对细胞活力和侵袭的抑制作用。我们发现了[物质名称]与铁死亡之间的新联系，即[物质名称]敲低通过调节[相关蛋白名称]介导的脂质过氧化和铁代谢途径使U251细胞对铁死亡细胞死亡敏感。[具体实验]研究揭示，在[物质名称]敲低模型中肿瘤生长和Ki-67表达降低，肿瘤组织中[相关蛋白名称]水平下降。
结果突出了[物质名称]作为胶质母细胞瘤进展和铁死亡敏感性的关键调节因子，[相关蛋白名称]作为关键的下游效应器。我们的发现为驱动胶质母细胞瘤侵袭性的分子机制提供了新见解，并提出[物质名称]和[相关蛋白名称]作为对抗这种致命疾病的有希望的治疗靶点。
