Wang Ding, Wang Haiyang, Zheng Wenhao, Wang Heng, Yu Wenhua, Du Quan
Department of Neurosurgery, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, Zhejiang, People's Republic of China.
J Cell Mol Med. 2025 Jul;29(13):e70711. doi: 10.1111/jcmm.70711.
Glioma is the most common and highly invasive type of brain cancer in the central nervous system, characterised by a low survival rate and poor prognosis. The role of SERPINB6 has been proven crucial in programmed necrosis and cancer progression. However, its role in glioma has not yet been clearly defined. This study utilised bioinformatics methods and in vitro and in vivo experiments to assess the expression, function and potential mechanisms of SERPINB6 in the development of glioma. Our study found that SERPINB6 plays a carcinogenic role in glioma, and its expression level is significantly negatively correlated with patient prognosis. The study also found that inhibiting SERPINB6 expression can hinder the epithelial-mesenchymal transition (EMT) of glioma cells. Conversely, overexpression of SERPINB6 aggravated the occurrence of EMT. Particularly noteworthy is the mechanism of SERPINB6 in promoting EMT in glioma, which is achieved through the activation of the PI3K/AKT/mTOR signalling pathway. By activating the PI3K/AKT/mTOR pathway, SERPINB6 promotes EMT in glioma, demonstrating its great potential as a new target for glioma treatment.
神经胶质瘤是中枢神经系统中最常见且具有高度侵袭性的脑癌类型,其特点是生存率低且预后差。已证实丝氨酸蛋白酶抑制剂B6(SERPINB6)在程序性坏死和癌症进展中起关键作用。然而,其在神经胶质瘤中的作用尚未明确界定。本研究利用生物信息学方法以及体外和体内实验,评估SERPINB6在神经胶质瘤发生发展中的表达、功能及潜在机制。我们的研究发现,SERPINB6在神经胶质瘤中起致癌作用,其表达水平与患者预后显著负相关。该研究还发现,抑制SERPINB6表达可阻碍神经胶质瘤细胞的上皮-间质转化(EMT)。相反,SERPINB6的过表达会加剧EMT的发生。特别值得注意的是,SERPINB6在神经胶质瘤中促进EMT的机制是通过激活PI3K/AKT/mTOR信号通路实现的。通过激活PI3K/AKT/mTOR通路,SERPINB6促进神经胶质瘤中的EMT,表明其作为神经胶质瘤治疗新靶点具有巨大潜力。