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Published on: March 30, 2019
miR-139-5p Inhibits Lung Adenocarcinoma Cell Proliferation, Migration, and Invasion by Targeting MAD2L1
Jianfeng Li1, Xi He1, Xiaotang Wu2
1Department of Thoracic Surgery, Tangshan People's Hospital, Tangshan, China.
Background:
miR-139-5p is lowly expressed in various human cancers and exerts its antitumor effect through different molecular mechanisms, yet the molecular mechanism of miR-139-5p in lung adenocarcinoma (LUAD) remains to be further elucidated. The study is aimed at investigating the role and the regulatory mechanism of miR-139-5p in LUAD progression.
Methods:
Differential analysis was performed on miRNA expression data in the TCGA-LUAD dataset. qRT-PCR was employed to detect the transcription levels of miR-139-5p and MAD2L1 in LUAD cells, while western blot was carried out for the detection of MAD2L1 protein expression. CCK-8 and Transwell assays were implemented to assess LUAD cell proliferation, migration, and invasion. A dual-luciferase reporter gene assay was conducted to verify the direct targeting relationship between miR-139-5p and MAD2L1.
Results:
miR-139-5p was significantly downregulated in LUAD cells in comparison with that in human normal bronchial epithelial cells. Overexpressing miR-139-5p inhibited LUAD cell proliferation, migration, and invasion, while opposite results could be observed when miR-139-5p was inhibited. MAD2L1 was identified as a direct target of miR-139-5p in LUAD. Besides, the inhibitory effect of miR-139-5p overexpression on LUAD cell proliferation, migration, and invasion was attenuated by overexpressing MAD2L1.
Conclusion:
Our study suggests that miR-139-5p is lowly expressed in LUAD cells and inhibits LUAD cell proliferation, migration, and invasion by targeted suppressing MAD2L1 expression. It is of potential significance for the prognosis and treatment of LUAD.
Insights
MicroRNA-139-5p is downregulated in lung adenocarcinoma (LUAD), inhibiting cancer progression by targeting MAD2L1. Restoring miR-139-5p levels may offer a new therapeutic strategy for LUAD patients.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNA-139-5p (miR-139-5p) exhibits antitumor properties in various cancers, but its specific role in lung adenocarcinoma (LUAD) requires further investigation.
- Understanding the molecular mechanisms of miR-139-5p in LUAD is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role of miR-139-5p in the progression of lung adenocarcinoma (LUAD).
- To elucidate the molecular mechanism by which miR-139-5p regulates LUAD progression.
Main Methods:
- Differential gene expression analysis using TCGA-LUAD dataset.
- Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot to assess miR-139-5p and MAD2L1 levels.
- Cell proliferation, migration, and invasion assays (CCK-8, Transwell).
- Dual-luciferase reporter assay to confirm direct targeting.
Main Results:
- miR-139-5p was significantly downregulated in LUAD tissues compared to normal tissues.
- Overexpression of miR-139-5p suppressed LUAD cell proliferation, migration, and invasion.
- MAD2L1 was identified as a direct target of miR-139-5p, and its overexpression attenuated the inhibitory effects of miR-139-5p.
Conclusions:
- miR-139-5p acts as a tumor suppressor in LUAD by inhibiting cell proliferation, migration, and invasion through the targeted suppression of MAD2L1.
- miR-139-5p holds potential as a prognostic biomarker and therapeutic target for LUAD.
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