Effect of miR-216a-3p on lung cancer hasn’t been investigated. Here, we explored its effects on lung cancer. MiR-216a-3p expression in lung cancer tissues and cells was detected by RT-qPCR. The target gene of miR-216a-3p was predicted by bioinformatics and confirmed by luciferase-reporter assay. After transfection, cell viability, migration, invasion, proliferation, and apoptosis were detected by MTT, scratch, transwell, colony formation, and flow cytometry. The expressions of COPB2 and apoptosis-related factors were detected by RT-qPCR or western blot. MiR-216a-3p was low-expressed and COPB2 was high-expressed in lung cancer tissues and cells. MiR-216a-3p targeted COPB2 and regulated its expression. MiR-216a-3p inhibited lung cancer cell viability, migration, invasion, and proliferation, while promoted apoptosis. Effect of miR-216a-3p on lung cancer was reversed by COPB2. MiR-216a-3p regulated proliferation, apoptosis, migration, and invasion of lung cancer cells via targeting COPB2.

尚未研究miR-216a-3p对肺癌的作用。在这里，我们探讨了其对肺癌的影响。RT-qPCR检测MiR-216a-3p在肺癌组织和细胞中的表达。miR-216a-3p的靶基因已通过生物信息学预测，并通过萤光素酶报告基因测定得以证实。转染后，通过MTT，刮擦，转运，集落形成和流式细胞术检测细胞活力，迁移，侵袭，增殖和凋亡。RT-qPCR或western blot检测COPB2及凋亡相关因子的表达。MiR-216a-3p在肺癌组织和细胞中低表达，而COPB2在肺癌组织和细胞中高表达。MiR-216a-3p靶向COPB2并调节其表达。MiR-216a-3p抑制肺癌细胞的活力，迁移，侵袭和增殖，同时促进细胞凋亡。miR-216a-3p对肺癌的作用被COPB2逆转。MiR-216a-3p通过靶向COPB2调节肺癌细胞的增殖，凋亡，迁移和侵袭。