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首页> 外文期刊>RSC Advances >LncRNA CASC2 inhibits autophagy and promotes apoptosis in non-small cell lung cancer cells via regulating the miR-214/TRIM16 axis
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LncRNA CASC2 inhibits autophagy and promotes apoptosis in non-small cell lung cancer cells via regulating the miR-214/TRIM16 axis

机译：LNCRNA Casc2通过调节MiR-214 / Trim16轴来抑制自噬并促进非小细胞肺癌细胞的细胞凋亡

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Background: Dysregulated long noncoding RNAs (lncRNAs) have been frequently observed in various cancers including non-small cell lung cancer (NSCLC) and are closely associated with cancer progression. Previous studies also found that low expression of lncRNA cancer susceptibility candidate 2 (CASC2) functioned as a tumor suppressor in NSCLC. Our study aimed to explore the detailed molecular mechanism of CASC2 involved in NSCLC progression. Methods: The expressions of CASC2, tripartite motif-containing protein 16 (TRIM16) and miR-214 in NSCLC tissues and cells were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) or western blot. Flow cytometry analysis was performed to evaluate apoptosis. Autophagy was assessed using green fluorescent protein microtubule-associated protein 1 light chain 3 (GFP-LC3) puncta analysis, acridine orange (AO) staining and western blot. Luciferase reporter assay, RNA immunoprecipitation (RIP), RNA pull-down and immunofluorescence staining were employed to explore the association between CASC2, TRIM16 and miR-214. Results: CASC2 and TRIM16 expressions were significantly downregulated and miR-214 expression was dramatically upregulated in NSCLC tissues and cells. Overexpression of CASC2 induced apoptosis and inhibited autophagy in NSCLC cells. miR-214 was bound to CASC2 and its knockdown reversed the regulatory effect of CASC2 inhibition on apoptosis and autophagy in NSCLC cells. Moreover, TRIM16 was validated as a target of miR-214 and its interference attenuated miR-214 knockdown-mediated promotion of apoptosis and inhibition of autophagy. Besides, CASC2 enhanced TRIM16 expression through functioning as a competing endogenous RNA (ceRNA) for miR-214 in NSCLC cells. Conclusion: lncRNA CASC2 inhibited autophagy and promoted apoptosis in NSCLC cells via regulating the miR-214/TRIM16 axis, shedding light on the mechanism underlying NSCLC carcinogenesis.
机译：背景：在包括非小细胞肺癌（NSCLC）的各种癌症中，经常观察到呼吸困难的长rNA（LNCRNA），并且与癌症进展密切相关。之前的研究还发现，在NSCLC中用作肿瘤抑制剂的LNCRNA癌敏感性候选候选2（CASC2）的低表达。我们的研究旨在探讨Casc2参与NSCLC进展的详细分子机制。方法：通过逆转录定量聚合酶链反应（RT-QPCR）或Western印迹检测Casc2，含三方含有蛋白质16（Trim16）和MiR-214的Casc2，含三方基序蛋白质16（Trim16）和miR-214。进行流式细胞术分析以评估细胞凋亡。使用绿色荧光蛋白微管相关蛋白1轻链3（GFP-LC3）斑块分析，吖啶橙（AO）染色和Western印迹进行评估自噬。荧光素酶报告器测定，RNA免疫沉淀（RIP），RNA下拉和免疫荧光染色被用来探讨Casc2，Trim16和miR-214之间的关联。结果：Casc2和Trim16表达明显下调，MiR-214表达在NSCLC组织和细胞中显着上调。 CASC2诱导细胞凋亡的过度表达和NSCLC细胞中的抑制自噬。 miR-214与Casc2结合，其敲低扭转了Casc2抑制对NSCLC细胞凋亡和自噬的调节作用。此外，Trim16被验证为miR-214的靶标，其干扰衰减miR-214敲低介导的凋亡促进和抑制自噬。此外，Casc2增强了Trim16表达，通过用作NSCLC细胞中miR-214的竞争内源性RNA（Cerna）。结论：LNCRNA CASC2通过调节MIR-214 / TRIM16轴，在NSCLC致癌物质下面的机制上脱落光抑制了NSCLC细胞中的自噬和促进了凋亡。

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  • 来源
    《RSC Advances》 |2018年第71期|共10页
  • 作者

    Li Qian; Chen Kai; Dong Rong; Lu Hengxiao;

  • 作者单位

    Peoples Hosp Rizhao Dept Resp Rizhao 276800 Peoples R China;

    Peoples Hosp Rizhao Dept Resp Rizhao 276800 Peoples R China;

    Peoples Hosp Rizhao Dept Resp Rizhao 276800 Peoples R China;

    Weifang Peoples Hosp Dept Thorac Surg 151 Guangwen St Weifang 261041 Peoples R China;

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  • 正文语种 eng
  • 中图分类 化学;
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