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Mir-451 inhibits proliferation and migration of non-small cell lung cancer cells via targeting LKB1/AMPK
1Department of Respiratory Medicine, General Hospital of the North China Petroleum Administration, Renqiu, China. 15303175650@163.com.
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.
Insights
MicroRNA-451 (miR-451) influences non-small cell lung cancer (NSCLC) cell proliferation and migration. miR-451 negatively correlates with liver kinase B1 (LKB1)/adenosine monophosphate-activated protein kinase (AMPK) signaling, suggesting a therapeutic target.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality.
- MicroRNAs (miRNAs) play critical roles in cancer development and progression.
- Dysregulation of specific miRNAs, such as miR-451, is implicated in NSCLC pathogenesis.
Purpose of the Study:
- To investigate the role of miR-451 in NSCLC cell proliferation and apoptosis.
- To elucidate the regulatory mechanism of miR-451 on liver kinase B1 (LKB1) and adenosine monophosphate-activated protein kinase (AMPK) signaling pathways.
- To explore the potential of targeting miR-451 for NSCLC treatment.
Main Methods:
- Utilized A549 NSCLC cells cultured under different conditions (control, miR-451 mimic, miR-451 inhibitor).
- Assessed cell proliferation and migration using cell counting kit-8 (CCK8) and Transwell assays.
- Quantified the expression levels of LKB1 and AMPK via Reverse Transcription-Polymerase Chain Reaction (RT-PCR).
Main Results:
- miR-451 mimic significantly decreased cell migration, while miR-451 inhibitor increased it (p < 0.05).
- Cell proliferation was altered by miR-451 modulation, with significant differences observed among groups (p < 0.05).
- miR-451 mimic led to decreased expression of LKB1 and AMPK, whereas miR-451 inhibitor showed no significant difference compared to controls (p > 0.05).
Conclusions:
- miR-451 negatively correlates with LKB1/AMPK signaling in NSCLC.
- The LKB1/AMPK pathway is involved in NSCLC cell metabolism.
- miR-451 may exert its tumor-suppressive effects in NSCLC by regulating the LKB1/AMPK pathway.
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