LINC00839/miR-519d-3p/JMJD6轴调控肺癌细胞的活力、凋亡、迁移和侵袭性。

IF 1.7 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Folia histochemica et cytobiologica Pub Date : 2021-01-01 Epub Date: 2021-11-04 DOI:10.5603/FHC.a2021.0022
Xiaoyan Yu, Yifei Jiang, Xun Hu, Xiang Ge
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引用次数: 5

摘要

长链非编码rna与肺癌的进展有关。LINC00839在骨肉瘤、乳腺癌和肺癌(LC)中表达异常。作为一种上调的lncRNA, LINC00839在肺癌中的作用尚不清楚。材料与方法:RT-qPCR检测LINC00839、miR-519d-3p、JMJD6的RNA表达,Western blot检测JMJD6蛋白表达。同时,用CCK-8法检测siNC、siLINC00839、oeNC、oeLINC00839、NC模拟物、miR-519d-3p模拟物和siJMJD6转染oeLINC00839的A549和H460 LC细胞的活力,用流式细胞术检测细胞凋亡。同时,利用transwell分析了迁移性和侵袭性。通过荧光素酶报告基因检测检测LINC00839与miR-519d-3p、miR-519d-3p和JMJD6之间的结合。结果:LINC00839在LC细胞中表达上调,其表达下调导致细胞活力、迁移能力和侵袭能力下降,细胞凋亡增加。MiR-519d-3p是LINC00839的靶基因,过表达LINC00839可降低其表达。miR-519d-3p直接靶向并在mRNA和蛋白表达水平上抑制JMJD6。此外,miR-519d-3p过表达导致LC细胞活力、迁移性、侵袭性低,但凋亡率高。此外,过表达LINC00839可上调JMJD6 mRNA和蛋白的表达。LINC00839竞争性地滤除miR-519d-3p,增加A549和H460肺癌细胞中JMJD6的表达、LC细胞活力、侵袭、迁移能力,并降低凋亡率,这些在JMJD6敲除后受到抑制。结论:LINC00839/miR-519d-3p/JMJD6轴介导H460肺癌细胞的细胞活力、凋亡、迁移和侵袭。
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LINC00839/miR-519d-3p/JMJD6 axis modulated cell viability, apoptosis, migration and invasiveness of lung cancer cells.

Introduction: Long noncoding RNAs are associated with progressions of lung cancer. LINC00839 has been dysregulated in osteosarcoma, breast cancer and lung cancer (LC). As an upregulated lncRNA, the roles of LINC00839 in lung cancer remain unclear.

Material and methods: RNA expressions of LINC00839, miR-519d-3p and JMJD6 were assessed using RT-qPCR and JMJD6 protein expression were analyzed through Western blot. Meanwhile, viabilities of A549 and H460 LC cells transfected by siNC, siLINC00839, oeNC, oeLINC00839, NC mimics, miR-519d-3p mimics and oeLINC00839 with siJMJD6 were examined with CCK-8 assay while apoptosis was examined using flow cytometry. Meanwhile, migration and invasiveness were analyzed using transwell assays. Bindings between LINC00839 and miR-519d-3p, miR-519d-3p and JMJD6 were measured by luciferase reporter assays.

Results: LINC00839 was upregulated in LC cells and its knockdown resulted in reduced cell viability, migratory ability and invasion with increased cell apoptosis. MiR-519d-3p was the target gene of LINC00839 and its expression was reduced by LINC00839 overexpression. JMJD6 was directly targeted and suppressed at the level of mRNA and protein expression by miR-519d-3p. Moreover, miR-519d-3p overexpression resulted in low LC cell viability, migration, invasiveness but a high apoptosis rate. Furthermore, mRNA and protein expressions of JMJD6 were upregulated by LINC00839 overexpression. LINC00839 competitively sponged miR-519d-3p, increasing JMJD6 expression, LC cell viability, invasion, migratory abilities and decreasing apoptosis rates in A549 and H460 lung cancer cells, which were hindered after JMJD6 knockdown.

Conclusions: LINC00839/miR-519d-3p/JMJD6 axis mediated cell viability, apoptosis, and migration and invasiveness of H460 lung cancer cells.

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来源期刊
Folia histochemica et cytobiologica
Folia histochemica et cytobiologica 生物-生化与分子生物学
CiteScore
2.80
自引率
6.70%
发文量
56
审稿时长
6-12 weeks
期刊介绍: "Folia Histochemica et Cytobiologica" is an international, English-language journal publishing articles in the areas of histochemistry, cytochemistry and cell & tissue biology. "Folia Histochemica et Cytobiologica" was established in 1963 under the title: ‘Folia Histochemica et Cytochemica’ by the Polish Histochemical and Cytochemical Society as a journal devoted to the rapidly developing fields of histochemistry and cytochemistry. In 1984, the profile of the journal was broadened to accommodate papers dealing with cell and tissue biology, and the title was accordingly changed to "Folia Histochemica et Cytobiologica". "Folia Histochemica et Cytobiologica" is published quarterly, one volume a year, by the Polish Histochemical and Cytochemical Society.
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