Mir-451 inhibits proliferation and migration of non-small cell lung cancer cells via targeting LKB1/AMPK

Y. Liu, H. Li, L.-H. Li, J.-B. Tang, Y.-L. Sheng

Department of Respiratory Medicine, General Hospital of the North China Petroleum Administration, Renqiu, China. 15303175650@163.com

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• Geriatrics

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, 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.

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 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).

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.

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