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LncRNA SNHG14 promotes non-small cell lung cancer progression by sponging miR-382-5p
Frontiers in Life Science Pub Date : 2020-07-27 , DOI: 10.1080/26895293.2020.1790431
Yayan Zhou 1 , Gang Xu 1 , Minjie Fang 1 , Shihai Wu 1 , Zhanghong Tan 1 , Rencui Quan 1 , Zihuang Li 1 , Xianming Li 1
Affiliation  

Long non-coding RNAs (lncRNAs) are involved in development of non-small cell lung cancer (NSCLC) by interacting with microRNAs (miRNAs) and/or mRNAs. However, the function of most lncRNAs in NSCLC remains unclear. Reverse transcription-quantitative PCR (RT-qPCR) and western blot were applied for detection of mRNA/miRNA and protein level. Interaction between LncRNA small nucleolar RNA host gene 14 (SNHG14) and miR-382-5p was validated by dual luciferase reporter assay. Cell proliferation and apoptosis was detected using Cell Counting Kit 8 (CCK8) and Flow cytometry, while cell migration and invasion was detected by scratch assay and Transwell assay. SNHG14 was upregulated in NSCLC tissues and cell lines. SNHG14 silencing reduced proliferation, migration and invasion, and induced apoptosis in A549 cells. SNHG14 was negatively correlated with miR-382-5p in NSCLC tissues, SNHG14 and miR-382-5p negatively regulated each other in A549 cells. SNHG14 promoted expression of miR-382-5p target genes, including LIM-only protein 3 (LMO3) and SET domain containing lysine methyltransferase 8 (SETD8), in A549 cells. miR-382-5p inhibition reversed SNHG14 knockdown-induced increase in apoptosis and decrease in proliferation, migration and invasion. SNHG14 was correlated with SETD8 and LMO3 in NSCLC tissues. Collectively, SNHG14 promoted NSCLC proliferation, migration and invasion, while inhibited apoptosis by sponging miR-382-5p in A549 cells.

Abbreviations: CCK8: Cell Counting Kit 8; LMO3: LIM-only protein 3; lncRNAs: long non-coding RNAs; miRNAs: microRNAs; NSCLC: non-small cell lung cancer; RT-qPCR: reverse transcription-quantitative PCR; SNHG14: LncRNA small nucleolar RNA host gene 14; SETD8: SET domain containing lysine methyltransferase 8.



中文翻译:

LncRNA SNHG14通过刺激miR-382-5p促进非小细胞肺癌的进展

长的非编码RNA(lncRNA)通过与microRNA(miRNA)和/或mRNA相互作用而参与非小细胞肺癌(NSCLC)的发展。但是,大多数lncRNA在NSCLC中的功能仍不清楚。应用逆转录定量PCR(RT-qPCR)和western blot检测mRNA / miRNA和蛋白水平。LncRNA小核仁RNA宿主基因14(SNHG14)和miR-382-5p之间的相互作用已通过双重萤光素酶报告基因检测验证。使用细胞计数试剂盒8(CCK8)和流式细胞仪检测细胞增殖和凋亡,而通过划痕法和Transwell法检测细胞迁移和侵袭。SNHG14在NSCLC组织和细胞系中上调。SNHG14沉默减少增殖,迁移和入侵,并诱导A549细胞凋亡。SNHG14与NSCLC组织中的miR-382-5p呈负相关,SNHG14和miR-382-5p在A549细胞中彼此呈负相关。SNHG14促进了miR-382-5p靶基因在A549细胞中的表达,包括仅LIM蛋白3(LMO3)和包含赖氨酸甲基转移酶8(SETD8)的SET结构域。miR-382-5p抑制可逆转SNHG14敲低诱导的细胞凋亡增加,并减少增殖,迁移和侵袭。SNHG14与NSCLC组织中的SETD8和LMO3相关。SNHG14共同促进NSCLC增殖,迁移和侵袭,同时通过在A549细胞中使miR-382-5p海绵化来抑制细胞凋亡。包括A549细胞中仅LIM的蛋白质3(LMO3)和包含赖氨酸甲基转移酶8的SET结构域(SETD8)。miR-382-5p抑制可逆转SNHG14敲低诱导的细胞凋亡增加,并减少增殖,迁移和侵袭。SNHG14与NSCLC组织中的SETD8和LMO3相关。SNHG14共同促进NSCLC增殖,迁移和侵袭,同时通过在A549细胞中使miR-382-5p海绵化来抑制细胞凋亡。包括A549细胞中仅LIM的蛋白质3(LMO3)和包含赖氨酸甲基转移酶8的SET结构域(SETD8)。miR-382-5p抑制可逆转SNHG14敲低诱导的细胞凋亡增加,并减少增殖,迁移和侵袭。SNHG14与NSCLC组织中的SETD8和LMO3相关。SNHG14共同促进NSCLC增殖,迁移和侵袭,同时通过在A549细胞中使miR-382-5p海绵化来抑制细胞凋亡。

缩写: CCK8:细胞计数试剂盒8;LMO3:仅LIM蛋白3;lncRNA:长的非编码RNA;miRNA:microRNA;NSCLC:非小细胞肺癌;RT-qPCR:逆转录定量PCR;SNHG14:LncRNA小核仁RNA宿主基因14;SETD8:包含赖氨酸甲基转移酶8的SET结构域。

更新日期:2020-07-27
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