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首页> 外文期刊>RSC Advances >Long non-coding RNA MEG3 inhibits cell proliferation, migration, invasion and enhances apoptosis in non-small cell lung cancer cells by regulating the miR-31-5p/TIMP3 axis
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Long non-coding RNA MEG3 inhibits cell proliferation, migration, invasion and enhances apoptosis in non-small cell lung cancer cells by regulating the miR-31-5p/TIMP3 axis

机译：通过调节MiR-31-5P / TIMP3轴，长期非编码RNA MEG3抑制细胞增殖，迁移，侵袭，增强非小细胞肺癌细胞的细胞凋亡

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Non-small cell lung cancer (NSCLC) is a malignant lung cancer and accounts for 80% of lung cancer-related deaths. Long non-coding RNA maternally expressed gene 3 (MEG3) has been identified as a tumor suppressor in multiple cancers. However, the regulatory mechanism of MEG3 in NSCLC development is still largely unknown. The expression levels of MEG3, microRNA-31-5p (miR-31-5p) and tissue inhibitor of metalloproteinase 3 (TIMP3) in NSCLC tumors and cells were measured by quantitative real time polymerase chain reaction (qRT-PCR). Cell viability, apoptosis, migration and invasion were detected by cell counting kit-8 (CCK-8), flow cytometry, western blotting and transwell assays, respectively. Xenograft mouse models were established by subcutaneously injecting NSCLC cells stably transfected with Lenti-pcDNA or Lenti-MEG3. The interaction between miR-31-5p and MEG3 or TIMP3 was validated by luciferase reporter and RNA immunoprecipitation (RIP) assays. MEG3 and TIMP3 levels were up-regulated, whereas miR-31-5p expression was down-regulated in NSCLC tumors and cells compared with normal tissues and cells. Overexpression of MEG3 repressed cell proliferation, migration and invasion, but induced apoptosis in NSCLC cells. More importantly, MEG3 effectively hindered tumor growth in vivo. Next, luciferase reporter and RIP assays confirmed the interaction between miR-31-5p and MEG3 or TIMP3. Pearson's correlation coefficient revealed that miR-31-5p was inversely correlated with MEG3 or TIMP3. Rescue experiments indicated that MEG3 regulated TIMP3 expression by sponging miR-31-5p in NSCLC cells. Thus, MEG3 inhibited cell proliferation, migration and invasion, but enhanced apoptosis in NSCLC cells through up-regulating TIMP3 expression by regulating miR-31-5p, indicating novel biomarkers for the therapy of NSCLC.
机译：非小细胞肺癌（NSCLC）是恶性肺癌，占肺癌 - 相关死亡的80％。长的非编码RNA母系表达基因3（MEG3）已经被鉴定为在多种癌症肿瘤抑制。然而，MEG3在非小细胞肺癌发展的调控机制仍知之甚少。 MEG3的表达水平，微小RNA-31-5p（的miR-31-5p）和非小细胞肺癌肿瘤和细胞基质金属蛋白酶3（TIMP3）的组织抑制剂通过定量实时聚合酶链式反应（qRT-PCR）来测定。分别细胞活力，凋亡，迁移和侵袭通过细胞计数试剂盒-8（CCK-8）检测，流式细胞术，Western印迹和转孔试验中，。异种移植物小鼠模型，通过皮下注射NSCLC细胞的Lenti-的pcDNA或伦蒂-MEG3稳定转染建立的。的miR-31-5p和MEG3或TIMP3之间的相互作用通过萤光素酶报道和RNA免疫沉淀（RIP）测定法验证。 MEG3和TIMP3水平上调，在NSCLC肿瘤和细胞而miR-31-5p表达下调与正常组织和细胞进行比较。 MEG3的过表达抑制细胞的增殖，迁移和侵袭，但诱导的细胞凋亡中的NSCLC细胞。更重要的是，有效地MEG3阻碍体内肿瘤生长。接着，萤光素酶报道和RIP分析证实的miR-31-5p和MEG3或TIMP3之间的相互作用。 Pearson相关系数表明的miR-31-5p呈负MEG3或TIMP3相关。拯救实验通过在NSCLC细胞揩的miR-31-5p表明MEG3调节TIMP3表达。因此，MEG3通过调节的miR-31-5p，指示用于非小细胞肺癌的治疗中的生物标志物的新通过上调TIMP3表达抑制细胞的增殖，迁移和侵袭，但增强的细胞凋亡的NSCLC细胞。

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    《RSC Advances》 |2019年第65期|共9页
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