Yu Xiaoyan, Jiang Yifei, Hu Xun, Ge Xiang
The Second Affiliated Hospital of Jiaxing University, Pulmonary and Critical Care Medicine, Jiaxing, China.
Folia Histochem Cytobiol. 2021;59(4):271-281. doi: 10.5603/FHC.a2021.0022. Epub 2021 Nov 4.
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.
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.
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.
LINC00839/miR-519d-3p/JMJD6 axis mediated cell viability, apoptosis, and migration and invasiveness of H460 lung cancer cells.
长链非编码RNA与肺癌进展相关。LINC00839在骨肉瘤、乳腺癌和肺癌（LC）中表达失调。作为一种上调的lncRNA，LINC00839在肺癌中的作用尚不清楚。
采用RT-qPCR评估LINC00839、miR-519d-3p和JMJD6的RNA表达，通过蛋白质免疫印迹分析JMJD6蛋白表达。同时，用CCK-8法检测转染siNC、siLINC00839、oeNC、oeLINC00839、NC mimics、miR-519d-3p mimics以及oeLINC00839与siJMJD6的A549和H460肺癌细胞的活力，用流式细胞术检测细胞凋亡。同时，用Transwell实验分析细胞迁移和侵袭能力。通过荧光素酶报告基因实验检测LINC00839与miR-519d-3p、miR-519d-3p与JMJD6之间的结合。
LINC00839在肺癌细胞中上调，敲低其表达导致细胞活力、迁移能力和侵袭能力降低，细胞凋亡增加。miR-519d-3p是LINC00839的靶基因，LINC00839过表达使其表达降低。miR-519d-3p直接靶向JMJD6并在mRNA和蛋白表达水平抑制其表达。此外，miR-519d-3p过表达导致肺癌细胞活力、迁移和侵袭能力降低，但凋亡率升高。此外，LINC00839过表达上调JMJD6的mRNA和蛋白表达。LINC00839竞争性结合miR-519d-3p，增加JMJD6表达、肺癌细胞活力、侵袭和迁移能力，降低A549和H460肺癌细胞的凋亡率，敲低JMJD6后上述作用受到抑制。
LINC00839/miR-519d-3p/JMJD6轴介导H460肺癌细胞的活力、凋亡、迁移和侵袭。
