Mir-451 inhibits proliferation and migration of non-small cell lung cancer cells via targeting LKB1/AMPK
Mir-451 inhibits proliferation and migration of non-small cell lung cancer cells via targeting LKB1/AMPK
复制标题
DOI：
10.26355/eurrev_201908_18657
复制
发表时间：
2019-01-01
影响因子：
3.3
通讯作者：
Sheng, Y. -L.
中科院分区：
文献类型：
--
作者：
Liu, Y.;Li, H.;Sheng, Y. -L.
目的：探讨微小核糖核酸（miR）-451通过调节肝激酶B1（LKB1）信号、激活腺苷酸激活蛋白激酶（AMPK）对非小细胞肺癌（NSCLC）细胞增殖和凋亡的影响。 材料与方法：将肺癌A549细胞分为对照组、对照组、对照组和对照组。 miR451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）实验检测三组细胞的增殖和迁移能力，以及LKB1和AMPK的表达。结果：与对照组相比，miR-451模拟组迁移细胞数明显下降，而miR-451组迁移细胞数明显下降。 抑制剂组显着增加，差异有统计学意义（p<0.05）。细胞培养7 d时，miR-451模拟组细胞增殖能力高于对照组，且对照组高于miR451模拟组，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模拟组LKB1和AMPK的表达显着降低，差异有统计学意义（p < 0.05）。 miR-451抑制剂组与对照组LKB1和AMPK活性差异无统计学意义（p>0.05）。结论：LKB1/AMPK可能参与NSCLC的细胞代谢，miR-451与LKB1/AMPK呈负相关。因此，miR-451可能通过调节LKB1/AMPK抑制NSCLC细胞增殖和迁移。
OBJECTIVE: 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).MATERIALS AND METHODS: Lung cancer A549 cells were divided into control group, miR451 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.RESULTS: 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 miR451 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). T he d ifferences i n a ctivities of LKB1 and AMPK between miR-451 inhibitor group and control group were not significant ( p > 0.05).CONCLUSIONS: 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.