摘要
星形细胞瘤是发生于神经外胚叶组织的原发性肿瘤,它生长迅速且呈恶性侵袭性发展,具有多种信号通路调控。其中典型的Wnt/β-catenin信号通路参与了星形细胞瘤的发展,当该通路被异常激活时,β-catenin进入细胞核内与T细胞因子(TCF)/淋巴样增强因子(LEF)形成功能复合物,进而激活下游基因如c-Myc、cyclin D1的表达,参与调控细胞增殖、迁移等一系列重要过程,从而导致星形细胞瘤的发生。程序性细胞死亡配体1(PD-L1)是一种免疫抑制受体配体,当程序性细胞死亡受体-1(PD-1)与其配体PD-L1结合后,抑制T细胞的活化,从而促进肿瘤细胞免疫逃逸。β-catenin失活能降低PD-L1的表达,β-catenin的激活可能促进星形细胞瘤的免疫逃逸。本文就β-catenin和PD-L1在弥漫浸润型星形细胞瘤发生发展中的作用及相关性进行概述。
Astrocytoma is a primary tumor that occurs in neuroectodermal tissue.It grows rapidly and develops in a malignant and invasive manner,and has multiple signal pathways regulation.The typical Wnt/β-catenin signal pathway is involved in the development of astrocytoma.When this pathway is abnormally activated,β-catenin enters the nucleus and forms a functional complex with T cell factor(TCF)/lymphoid enhancer factor(LEF),thereby activating the expression of downstream genes such as c-Myc and cyclin D1,participating in a series of important processes such as cell proliferation and migration,thus leading to the occurrence of astrocytoma.Programmed death-ligand 1(PD-L1)is an immunosuppressive receptor ligand.When programmed death(PD-1)binds to its ligand PD-L1,it inhibits the activation of T cells,thereby promoting tumor cell immune escape.The inactivation ofβ-catenin can reduce the expression of PD-L1,while the activation ofβ-catenin can promote the immune escape of astrocytoma.This article summarizes the role and correlation ofβ-catenin and PD-L1 in the occurrence and development of diffuse infiltrating astrocytoma.
作者
墙宏
石柳
高勤
QIANG Hong;SHI Liu;GAO Qin(Department of Pathology,Affiliated Hospital of Guizhou Medical University,Guiyang,Guizhou 550001,China;不详)
出处
《中国临床研究》
CAS
2023年第1期139-142,147,共5页
Chinese Journal of Clinical Research
基金
贵州省卫生健康委科学技术基金项目(gzwjkj2020-1-180)。
