Liu Y, Li H, Li L-H, Tang J-B, Sheng Y-L
Department of Respiratory Medicine, General Hospital of the North China Petroleum Administration, Renqiu, China.
Eur Rev Med Pharmacol Sci. 2019 Aug;23(3 Suppl):274-280. doi: 10.26355/eurrev_201908_18657.
To discuss the influence of micro ribonucleic acid (miR)-451 on cell proliferation and apoptosis of non-small cell lung cancer (NSCLC) by regulating liver kinase B1 (LKB1) signals and activating adenosine monophosphate-activated protein kinase (AMPK).
Lung cancer A549 cells were divided into control group, miR-451 mimic group, and miR-451 inhibitor group. The cell proliferation and migration ability, as well as the expression of LKB1 and AMPK in the three groups, were determined via Reverse Transcription-Polymerase Chain Reaction (RT-PCR), transwell assay, and cell counting kit-8 (CCK8) assay, respectively.
Compared with that in control group, the number of migrating cells evidently declined in miR-451 mimic group, while that in miR-451 inhibitor group was significantly increased, and the differences were statistically significant (p < 0.05). At 7 d of cell culture, the cell proliferation ability in miR-451 mimic group was higher than that in control group, while it was higher in control group than that in miR-451 mimic group, and there were significant differences among the three groups (p < 0.05). The expression of LKB1 and AMPK was significantly decreased in miR-451 mimic group compared with that in miR-451 inhibitor group and control group, and the differences had statistical significance (p < 0.05). The differences in activities of LKB1 and AMPK between miR-451 inhibitor group and control group were not significant (p > 0.05).
LKB1/AMPK can be involved in the cell metabolism of NSCLC and miR-451 is negatively correlated with LKB1/AMPK. Therefore, miR-451 may inhibit cell proliferation and migration of NSCLC via regulating LKB1/AMPK.
探讨微小核糖核酸(miR)-451通过调节肝激酶B1(LKB1)信号并激活腺苷酸活化蛋白激酶(AMPK)对非小细胞肺癌(NSCLC)细胞增殖和凋亡的影响。
将肺癌A549细胞分为对照组、miR-451模拟物组和miR-451抑制剂组。分别通过逆转录-聚合酶链反应(RT-PCR)、Transwell实验和细胞计数试剂盒-8(CCK8)实验测定三组细胞的增殖和迁移能力以及LKB1和AMPK的表达。
与对照组相比,miR-451模拟物组迁移细胞数量明显减少,而miR-451抑制剂组显著增加,差异具有统计学意义(p<0.05)。细胞培养7天时,miR-451模拟物组细胞增殖能力高于对照组,而对照组高于miR-451抑制剂组,三组间差异有统计学意义(p<0.05)。与miR-451抑制剂组和对照组相比,miR-451模拟物组LKB1和AMPK的表达明显降低,差异有统计学意义(p<0.05)。miR-451抑制剂组与对照组之间LKB1和AMPK活性差异不显著(p>0.05)。
LKB1/AMPK可参与NSCLC的细胞代谢,且miR-451与LKB1/AMPK呈负相关。因此,miR-451可能通过调节LKB1/AMPK抑制NSCLC细胞的增殖和迁移。