Related Experiment Video
Updated: Dec 3, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
miR-371b-5p promotes cell proliferation, migration and invasion in non-small cell lung cancer via SCAI
Xue Luo1, Xiaolei Zhang2, Jianming Peng1
1School of Medicine, Yangzhou Polytechnic College, Yangzhou, Jiangsu 225009, China.
Objective:
Multiple gene targets have been reported for treatment of non-small cell lung cancer (NSCLC), however, the accompanying genetic tolerance was reported increasingly. Therefore, it is important to find new biomarkers or therapeutic targets in treatment of NSCLC.
Methods:
The expression levels of miR-371b-5p were detected by qRT-PCR in NSCLC tissues and cell lines. To evaluate the effect of miR-371b-5p on NSCLC progression, we first transfected the miR-371b-5p inhibitor for construction of the miR-371b-5p down-regulated cell model. Then the cell proliferation, migration, invasion and cell apoptosis were detected. In addition, the expression levels of adhesion factors were detected. The target gene of miR-371b-5p was identified by bioinformatics analysis, and rescue experiment was conducted to validate the effect of miR-371b-5p on proliferation, migration and invasion of NSCLC.
Results:
Our findings revealed that the miR-371b-5p was overexpressed in NSCLC and could markedly promote the cell proliferation, migration and invasion. Expression levels of both intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were significantly down-regulated when treated by miR-371b-5p inhibitor. Moreover, dual-luciferase reporter assay showed that the miR-371b-5p targeted SCAI in regulation of cell proliferation, migration and invasion, and the expression of miR-371b-5p was negatively associated with SCAI in NSCLC tissues and cell lines. Rescue experiment revealed that the miR-371b-5p could rescue the effect of SCAI on cell proliferation, migration and invasion.
Conclusion:
Our results suggest that the miR-371b-5p and SCAI may serve as novel prognostic biomarkers and therapeutic targets for NSCLC.
Insights
MicroRNA-371b-5p promotes non-small cell lung cancer (NSCLC) progression by targeting SCAI. This microRNA and SCAI may offer new therapeutic targets and prognostic biomarkers for NSCLC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Non-small cell lung cancer (NSCLC) presents challenges due to increasing genetic resistance to existing therapies.
- Identification of novel biomarkers and therapeutic targets is crucial for effective NSCLC treatment.
Purpose of the Study:
- To investigate the role of miR-371b-5p in the progression of non-small cell lung cancer.
- To identify potential therapeutic targets and prognostic biomarkers for NSCLC.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to assess miR-371b-5p expression in NSCLC tissues and cell lines.
- Transfection with miR-371b-5p inhibitors to create a down-regulated cell model for functional assays.
- Assays for cell proliferation, migration, invasion, apoptosis, and adhesion molecule expression.
- Bioinformatics analysis and dual-luciferase reporter assays to identify miR-371b-5p targets.
- Rescue experiments to validate target gene function.
Main Results:
- miR-371b-5p was found to be overexpressed in NSCLC, promoting cell proliferation, migration, and invasion.
- Down-regulation of miR-371b-5p led to decreased expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1).
- miR-371b-5p directly targets SCAI, and its expression is inversely correlated with SCAI levels in NSCLC.
- Rescue experiments confirmed that miR-371b-5p modulates the effects of SCAI on NSCLC cell behavior.
Conclusions:
- miR-371b-5p plays a significant role in promoting NSCLC progression.
- SCAI acts as a target gene for miR-371b-5p in the context of NSCLC.
- Both miR-371b-5p and SCAI show potential as novel prognostic biomarkers and therapeutic targets for NSCLC.
Related Concept Videos
Abnormal Proliferation
Cancer Cell Migration through Invadopodia
Mitogens and the Cell Cycle
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...

