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Updated: Feb 14, 2026

Detection of Targetable Alterations in Non-small Cell Lung Cancer using Next-generation Sequencing
Published on: October 10, 2025
MicroRNA-30a suppresses non-small-cell lung cancer by targeting Myb-related protein B
Guo-Jun Geng1, Ying-Tao Yang2,3, Jie Jiang1
1Department of Thoracic Surgery, The First Hospital Affiliated to Xiamen University, Xiamen, Fujian 361003, P.R. China.
Abstract:
Non-small-cell lung cancer (NSCLC) is one of the leading causes of cancer mortality worldwide. A growing body of evidence indicates that microRNA (miR) have important and diverse roles in the proliferation, apoptosis and metastasis of human cancer cells. In the present study, the molecular regulation mechanism of miR-30a and its potential target, Myb-related protein B (MYBL2) was investigated in NSCLC. Reverse transcription-quantitative polymerase chain reaction results showed that miR-30a was significantly downregulated in NSCLC tissues compared with adjacent normal tissues (P<0.05). MYBL2 has a putative miR-30a target site in its 3'untranslated region according to previous data, prediction databases and TargetScan software. In the present study, a negative correlation was demonstrated between miR-30a and MYBL2 expression in NSCLC. Direct interaction between miR-30a and MYBL2 was also confirmed via a dual-luciferase reporter assay. miR-30a overexpression inhibited the growth of A549 and H460 cells via MTT and bromodeoxyuridine incorporation assays, whereas miR-30a downregulation promoted cell proliferation. In addition, miR-30a overexpression not only increased cell apoptosis and induced cell cycle arrest in A549 and H460 cell lines, but also attenuated tumor growth, and mRNA and protein expression levels of MYBL2. The present findings suggest that miR-30a may suppress NSCLC by targeting MYBL2.
Insights
MicroRNA-30a (miR-30a) is downregulated in non-small-cell lung cancer (NSCLC). Restoring miR-30a levels suppresses tumor growth by targeting Myb-related protein B (MYBL2), suggesting a therapeutic role for miR-30a in NSCLC.
Area of Science:
- Molecular Biology
- Oncology
Background:
- Non-small-cell lung cancer (NSCLC) is a major global cause of cancer mortality.
- MicroRNAs (miRNAs) play critical roles in cancer cell proliferation, apoptosis, and metastasis.
- Understanding miRNA regulation is crucial for developing novel cancer therapies.
Purpose of the Study:
- To investigate the molecular mechanism of miR-30a regulation in NSCLC.
- To identify and validate Myb-related protein B (MYBL2) as a direct target of miR-30a.
- To evaluate the functional impact of miR-30a/MYBL2 interaction on NSCLC progression.
Main Methods:
- Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to assess miR-30a expression.
- Bioinformatic analysis and dual-luciferase reporter assay to confirm miR-30a targeting of MYBL2.
- Cell proliferation assays (MTT, BrdU incorporation) and cell cycle analysis to evaluate miR-30a function.
- In vivo tumor growth assessment.
Main Results:
- miR-30a was significantly downregulated in NSCLC tissues compared to normal tissues.
- A negative correlation between miR-30a and MYBL2 expression was observed in NSCLC.
- Overexpression of miR-30a inhibited NSCLC cell proliferation, induced apoptosis, and caused cell cycle arrest.
- miR-30a overexpression attenuated tumor growth and reduced MYBL2 expression in vivo.
Conclusions:
- miR-30a acts as a tumor suppressor in NSCLC by directly targeting and downregulating MYBL2.
- Restoration of miR-30a levels may represent a potential therapeutic strategy for NSCLC.
- The miR-30a/MYBL2 axis is a key regulatory pathway in NSCLC pathogenesis.
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