Xiaoyan Yu1, Yifei Jiang1, Xun Hu1, Xiang Ge2. 1. The Second Affiliated Hospital of Jiaxing University, Pulmonary and Critical Care Medicine, Jiaxing, China. 2. The Second Affiliated Hospital of Jiaxing University, Pulmonary and Critical Care Medicine, Jiaxing, China. ugh12254@126.com.
Abstract
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.
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.