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Received:March 25, 2022 Published Online:January 20, 2023
Received:March 25, 2022 Published Online:January 20, 2023
中文摘要: 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、cyclinD1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。
Abstract:Astrocytomaisaprimarytumorthatoccursinneuroectodermaltissue.Itgrowsrapidlyanddevelopsinamalignantandinvasivemanner,andhasmultiplesignalpathwaysregulation.ThetypicalWnt/β-cateninsignalpathwayisinvolvedinthedevelopmentofastrocytoma.Whenthispathwayisabnormallyactivated,β-cateninentersthenucleusandformsafunctionalcomplexwithTcellfactor（TCF）/lymphoidenhancerfactor（LEF）,therebyactivatingtheexpressionofdownstreamgenessuchasc-MycandcyclinD1,participatinginaseriesofimportantprocessessuchascellproliferationandmigration,thusleadingtotheoccurrenceofastrocytoma.Programmeddeath-ligand1（PD-L1）isanimmunosuppressivereceptorligand.Whenprogrammeddeath（PD-1）bindstoitsligandPD-L1,itinhibitstheactivationofTcells,therebypromotingtumorcellimmuneescape.Theinactivationofβ-catenincanreducetheexpressionofPD-L1,whiletheactivationofβ-catenincanpromotetheimmuneescapeofastrocytoma.Thisarticlesummarizestheroleandcorrelationofβ-cateninandPD-L1intheoccurrenceanddevelopmentofdiffuseinfiltratingastrocytoma.
文章编号： 中图分类号：R739.41 文献标志码：A
基金项目:贵州省卫生健康委科学技术基金项目（gzwjkj2020-1-180）
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