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长链非编码RNA对胰腺癌侵袭转移分子机制的影响

徐建 潘燕妮 刘欣原 江建新

引用本文:
Citation:

长链非编码RNA对胰腺癌侵袭转移分子机制的影响

DOI: 10.3969/j.issn.1001-5256.2022.01.043
基金项目: 

国家自然科学基金 (81871965)

利益冲突声明:所有作者均声明不存在利益冲突。
作者贡献声明:徐建负责课题设计,资料分析,撰写论文;徐建、潘燕妮和刘欣原参与收集数据,修改论文;江建新负责拟定写作思路,指导撰写文章并最后定稿。
详细信息
    通信作者:

    江建新,rm002979@whu.edu.cn

Research advances in the molecular mechanism of long non-coding RNA in invasion and metastasis of pancreatic cancer

Research funding: 

National Natural Science Foundation of China (81871965)

  • 摘要: 胰腺癌是一种恶性程度极高的消化道肿瘤,由于其高度侵袭转移特性,使得目前胰腺癌患者的总体生存率仍非常低。长链非编码RNA(lncRNA)可通过表观遗传调控、转录调控或转录后调控等多种方式参与胰腺癌的发生发展及侵袭转移过程。lncRNA在胰腺癌中表达失调,并通过特定调控方式使其发生上皮间充质转化,进而引起肿瘤细胞生物学行为发生改变。本文就研究lncRNA在胰腺癌中促使其发生上皮间充质转化,作为ceRNA调控肿瘤的生物学功能,并通过调控肿瘤细胞铁死亡、自噬及外泌体等多途径影响胰腺癌发生侵袭转移进行简要综述,为胰腺癌的早期诊断及治疗提供理论依据和新的靶点。

     

  • 图  1  lncRNA协同miRNA调控下游靶点影响胰腺癌侵袭和转移机制

    注:A,lncRNA XIST作为ceRNA下调miR-113a,靶向调控EGFR促进胰腺癌侵袭转移;B,lncRNA ZEB2-AS1协同miR-204相互抑制,上调HMGB1机制;C,lnc00976通过下调miR-137,使OTUD7B上调,激活下游EGFR/MAPK信号通路;D,lncRNA PSMB8-AS1通过调控miR-382-3p,使下游靶基因STAT1上调;E,lncRNA OIP5-AS1作为海绵吸附miR-342-3p,调控并激活AKT/ERK信号通路;F,lcnRNA PVT1调控miR-619-5p激活Pygo2和ATG14;G,lcnRNA 00941调控miR-335-5p,上调ROCK1后激活LIMK1/Cofilin-1信号通路;H,lcnRNA CERS6-AS1通过竞争性结合miR-127,上调YWHAG并磷酸化RAF1,激活ERK信号通路。

    表  1  lncRNA协同miRNA调控下游靶点介导胰腺癌侵袭转移相关研究

    lncRNA名称 miRNA靶标 下游靶点/通路 协同方式
    lncRNA XIST(上调) miR-113a(下调) EGFR 海绵/诱饵[21]
    lncRNA ZEB2-AS1(上调) miR-204(下调) HMGB1 相互抑制[22]
    lnc00976(上调) miR-137(下调) OTUD7B,下游EGFR/MAPK信号通路 海绵/诱饵[23]
    lncRNA PSMB8-AS1(上调) miR-382-3p(下调) STAT1 海绵/诱饵[24]
    lncRNA OIP5-AS1(上调) miR-342-3p(下调) AKT/ERK信号通路 海绵/诱饵[25]
    lcnRNA PVT1(上调) miR-619-5p(下调) Pygo2、ATG14 海绵/诱饵[9]
    lcnRNA 00941(上调) miR-335-5p(下调) ROCK1,下游LIMK1/Cofilin-1信号通路 海绵/诱饵[26]
    lcnRNA CERS6-AS1(上调) miR-127(下调) YWHAG、p-RAF1,ERK信号通路 海绵/诱饵[27]
    下载: 导出CSV
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  • 收稿日期:  2021-05-27
  • 录用日期:  2021-07-20
  • 出版日期:  2022-01-20
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