实用肿瘤学杂志 ›› 2023, Vol. 37 ›› Issue (2): 123-129.doi: 10.11904/j.issn.1002-3070.2023.02.006

• 基础研究 • 上一篇    下一篇

lncRNA AP000487.1在食管癌中的作用及机制研究

刘静1, 褚艳杰1, 裴凤华1, 徐睿玲1, 王彦博2   

  1. 1.哈尔滨医科大学附属第二医院消化内科(哈尔滨 150086);
    2.哈尔滨医科大学附属肿瘤医院胸外科
  • 收稿日期:2022-11-07 修回日期:2023-02-01 发布日期:2023-05-30
  • 通讯作者: 王彦博,E-mail:wangyanbo_034@126.com
  • 作者简介:刘静,女,(1984-),博士,副教授,从事消化道肿瘤的基础研究。
  • 基金资助:
    黑龙江省省属高等学校基本科研业务费科研项目(编号:2022-KYYWF-0275)

Role and mechanism of lncRNA AP000487.1 in esophageal cancer

LIU Jing1, CHU Yanjie1, PEI Fenghua1, XU Ruiling1, WANG Yanbo2   

  1. 1. Department of Gastroenterology and Hepatology,The Second Affifiliated Hospital of Harbin Medical University,Harbin 150086,China;
    2. Department of Thoracic Surgery,Harbin Medical University Cancer Hospital
  • Received:2022-11-07 Revised:2023-02-01 Published:2023-05-30

摘要: 目的 探究与生存相关的lncRNA AP000487.1在食管癌发生发展中的作用及机制。方法 qRT-PCR验证与食管癌患者总生存期显著相关的lncRNA AP000696.1、LINC00689、LINC00900和AP000487.1在食管癌组织和细胞株中的表达情况;在食管癌细胞株ECA109和TE-1中过表达和沉默AP000487.1后,采用CCK-8实验检测细胞增殖、Transwell侵袭实验评估细胞侵袭、划痕实验检测细胞迁移;采用Western blot测定TLR/NF-κB信号通路相关蛋白的表达;qRT-PCR检测NF-κB活化后炎症因子的表达。结果 qRT-PCR结果显示AP000487.1在食管癌细胞株ECA109(P<0.001)、TE-1(P<0.001)和食管癌组织(P<0.001)中表达显著上调;CCK-8、Transwell侵袭实验及划痕实验结果显示,在ECA109和TE-1细胞中沉默AP000487.1后降低了食管癌细胞的增殖、侵袭以及迁移能力;过表达AP000487.1后,增强癌细胞的增殖、侵袭及迁移能力;Western blot测定通路相关蛋白,结果显示沉默AP000487.1后,可抑制TLR/NF-κB信号通路,并下调p-p65和p-IκB在TE-1细胞中的表达;qRT-PCR检测NF-κB信号通路活化后炎症因子的表达,与Smart silencer-NC相比,Smart silencer-AP000487.1组TNF-α(P<0.001)、IL-1β(P<0.01)、IL-6(P<0.01)表达明显下调。结论 AP000487.1在食管癌细胞株及癌组织中显著高表达,其异常表达通过调控TLR/NF-κB信号通路促进食管癌的增殖、侵袭和迁移。AP000487.1可能是食管癌的潜在治疗靶点。

关键词: 食管癌, lncRNA, AP000487.1, Toll样受体, NF-κB

Abstract: Objective To explore the role and mechanism of survival-related lncRNA AP000487.1 in the occurrence and development of esophageal cancer. Methods qRT-PCR was used to verify the expression of lncRNA AP000696.1,LINC00689,LINC00900 and AP000487.1 that significantly associated with overall survival of esophageal cancer patients in esophageal cancer tissues and cell lines.Cell proliferation was detected by CCK-8 assay,cell invasion was evaluated by Transwell invasion assay,and cell migration was detected by scratch assay.The expression of TLR/NF-κB signaling pathway related proteins was detected by Western blot and qRT-PCR. Results The expression of AP000487.1 was significantly up-regulated in ECA109 cells,TE-1 cells,and ESCA tissues(P<0.001).Silencing AP000487.1 in ECA109 cells and TE-1 cells significantly inhibited the proliferation,invasion and migration of ESCA cells.Overexpression of AP000487.1 significantly enhanced the proliferation,invasion and migration.Western blot was used to detect pathway-related proteins,and the results showed that silencing AP000487.1 could inhibit the TLR/NF-κB signaling pathway and down-regulate the expression of p-p65 and p-IκB in TE-1 cells;Compared with the Smart silencer-NC group,the expressions of TNF-α(P<0.001),IL-1β(P<0.01)and IL-6(P<0.01)in the Smart silencer-AP000487.1 group were significantly down-regulated. Conclusion AP000487.1 is highly expressed in esophageal cancer cell lines and tissues,and its abnormal expression promotes the proliferation,invasion and migration of ESCA by regulating the TLR/NF-κB signaling pathway.AP000487.1 may be a potential therapeutic target for ESCA.

Key words: Esophagus cancer, lncRNA AP000487.1, Toll-like receptor, NF-κB

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