SRSF1剪接失调在非小细胞肺癌致病机制中的研究进展  

Research progress on splicing dysfunction of SRSF1 in the pathogenesis of NSCLC

作　　者：武艳旭 葛海燕[1] 葛晓晓 李向阳[1] Wu Yanxu;Ge Haiyan;Ge Xiaoxiao;Li Xiangyang(Huadong Hospital Affiliated to Fudan University,Shanghai 200040,China)

机构地区：[1]复旦大学附属华东医院,上海200040

出　　处：《现代肿瘤医学》2020年第15期2727-2729,共3页Journal of Modern Oncology

摘　　要：选择性剪接是蛋白质多样性产生的一个关键步骤,异常的选择性剪接功能失调与癌症有关。不同组织出现疾病时显示特定模式剪接变异体,SRSF1通过调节靶基因的选择性剪接发挥作用。剪接因子的表达改变与肿瘤发生、发展及预后有关。SRSF1可能通过不同的信号传导通路及在肿瘤发病过程中的多个环节发挥其致瘤活性。目前已证实SRSF1在非小细胞肺癌(NSCLC)中表达上调,可作为其诊断标志以及治疗的重要靶点。尽管如此,我们对SRSF1在NSCLC中准确致病机制的认识仍是了了。因此,明确SRSF1选择性剪接功能失调的致病机制对NSCLC的诊治具有重要意义。Alternative splicing is a key step in the production of protein diversity,and abnormal alternative splicing is associated with multiple cancers.Splicing variants of a specific pattern are shown in different tissues when diseases occur,and SRSF1 plays a role by regulating the alternative splicing of target genes.The expression of splicing factors is related to the occurrence,development and prognosis of tumor.SRSF1 may exert its tumorigenic activity through different signal transduction pathways and multiple links in the tumorigenesis process.The upregulation of SRSF1 in non-small cell lung cancer(NSCLC)has been confirmed as an important target for diagnosis and treatment.Nevertheless,our understanding of the pathogenesis of SRSF1 in NSCLC remains elusive.It is important to figure out the pathogenesis of SRSF1 alternative splicing dysfunction to the diagnosis and treatment of NSCLC.

关 键 词：富含丝氨酸/精氨酸剪接因子1 选择性剪接功能失调 致病机制 

分 类 号：R734.2[医药卫生—肿瘤]