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中华腔镜泌尿外科杂志(电子版) ›› 2021, Vol. 15 ›› Issue (05) : 446 -449. doi: 10.3877/cma.j.issn.1674-3253.2021.05.025

综述

长链非编码RNA在前列腺癌中的作用及机制研究进展
刘泽林1, 郭佳1,()   
  1. 1. 430060 湖北,武汉大学人民医院泌尿外科
  • 收稿日期:2020-08-24 出版日期:2021-10-01
  • 通信作者: 郭佳
  • 基金资助:
    国家自然科学基金青年基金(81702539)

The role and mechanism of long non-coding RNAs in prostate cancer: an update

Zelin Liu1, Jia Guo1()   

  • Received:2020-08-24 Published:2021-10-01
  • Corresponding author: Jia Guo
引用本文:

刘泽林, 郭佳. 长链非编码RNA在前列腺癌中的作用及机制研究进展[J]. 中华腔镜泌尿外科杂志(电子版), 2021, 15(05): 446-449.

Zelin Liu, Jia Guo. The role and mechanism of long non-coding RNAs in prostate cancer: an update[J]. Chinese Journal of Endourology(Electronic Edition), 2021, 15(05): 446-449.

表1 不同长链非编码RNA调控前列腺癌的作用机制
作用方式 名称 作用机制 参考文献
促癌 ARLNC1 ARLNC1基因敲除抑制AR的表达、全局AR信号和PCa的生长 [13]
  FOXP4-AS1 通过结合miR-3184-5p上调FOXP4促进PCa生长 [18]
  HOXD-AS1 招募WDR5通过介导H3K4me3直接调控靶基因的表达,促进PCa的增殖、去势抵抗和化疗耐药 [27]
  HULLK 增加对激素的敏感性来推动CRPC进展 [28]
  LEF1-AS1 下调LEF1的表达抑制了EMT、细胞侵袭和PCa的迁移 [29]
  LncRNA-p21 将EZH2的功能由组蛋白甲基转移酶转换为非组蛋白甲基转移酶,从而使STAT3甲基化以促进PCa神经内分泌化(NED) [30]
  MALAT1 减弱miR-145-5p的表达,上调AKAP12,诱导PCa细胞对DTX的化疗耐药,促进了PCa细胞的增殖、迁移和侵袭 [20]
  MIR222HG 促进雄激素非依赖性细胞的生长,并抑制AR调节的双氢睾酮(DHT)诱导的激素敏感型前列腺癌(HSPC)LNCaP细胞中KLK3、TMPRSS2和FKBP5的表达,促进CRPC的发生 [31]
  NEAT1 沉默NEAT1抑制了CDC5L的转录活性,使ARGN诱导DNA损伤、扰乱细胞周期、抑制PCa细胞的增殖 [16]
  PCA3 1.通过控制AR依赖的信号转导和AR辅助因子及EMT相关基因的表达来调节细胞存活;2.通过吸附miR-218-5p,从而上调HMGB1的表达,促进PCa的进展 [11,19]
  PCAT1 1.与FKBP51结合,取代PHLPP/FKBP51/IKKα蛋白复合体,导致AKT和NF-κB信号的激活,促进CRPC进展;2.抑制BRCA2肿瘤抑制因子的表达,导致下游同源重组功能受损;3.通过上调cMyc蛋白水平促进PCa细胞增殖 [2,23]
  PCAT19 风险SNP介导的启动子增强子转换激活PCAT19-Long,PCAT19-Long与HNRNPAB相互作用,激活与PCa进展相关的细胞周期基因子集 [32]
  PRCAT38 PRCAT38和TMPRSS2的启动子与AR激活的增强子E1和E2形成染色质环,增强子E1或E2的敲除同时影响PRCAT38和TMPRSS2的转录,抑制细胞生长和迁移 [1]
  SLC45A3-ELK4 SLC45A3-ELK4融合RNA通过其转录本调控癌细胞的增殖 [33]
  ZEB1-AS1 与MLL1结合并将其募集到ZEB1的启动子区域,诱导其中的H3K4me3修饰,激活ZEB1转录。从而抑制肿瘤抑制因子miR200c,促进BMI1的表达,促进PCa细胞的增殖和迁移 [34]
抑癌 LBCS 通过与hnRNPK和AR mRNA形成复合物来抑制AR翻译效率,抑制PCa的去势抵抗 [22]
  MEG3 抑制miR-9-5p的表达,上调QKI-5蛋白的表达,降低PCa细胞的增殖、迁移和侵袭能力,增加细胞凋亡率 [35]
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