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Updated: Feb 22, 2026

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells
Published on: May 21, 2019
MicroRNA-107-5p suppresses non-small cell lung cancer by directly targeting oncogene epidermal growth factor receptor
Ping Wang1, Xiaomin Liu1, Yang Shao1,2
1Laboratory for Noncoding RNA & Cancer, School of Life Sciences, Shanghai University, Shanghai, China.
Abstract:
MicroRNAs (miRNAs) are dysregulated in cancers, including human non-small cell lung cancer (NSCLC). The function of MicroRNA-107-5p (miR-107-5p) in NSCLC is not fully elucidated. Epidermal growth factor receptor (EGFR) is a cancer-driven gene in tumorigenesis. In this study, we found that miR-107-5p was significantly decreased in NSCLC tissues and NSCLC cell lines. Moreover, our results indicated that miR-107-5p could suppress cell proliferation, inhibit metastasis, impede cell cycle, and promote apoptosis via directly targeting EGFR. We also investigated roles of miR-107-5p in vivo. The results showed that it could inhibit tumor growth. Therefore, our study demonstrated that miR-107-5p not only suppressed the progression in NSCLC cells by inhibiting the expression of EGFR, but also could be a promising and a new potential therapeutic target for lung cancer.
Insights
MicroRNA-107-5p (miR-107-5p) is decreased in non-small cell lung cancer (NSCLC). This microRNA suppresses tumor growth, proliferation, and metastasis by targeting the epidermal growth factor receptor (EGFR).
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are crucial regulators of gene expression, and their dysregulation is implicated in various cancers, including non-small cell lung cancer (NSCLC).
- The specific role of microRNA-107-5p (miR-107-5p) in the pathogenesis and progression of NSCLC remains incompletely understood.
- Epidermal growth factor receptor (EGFR) is a key oncogene driving tumorigenesis in several cancer types.
Purpose of the Study:
- To investigate the expression levels of miR-107-5p in NSCLC tissues and cell lines.
- To elucidate the functional role of miR-107-5p in NSCLC progression, including its effects on cell proliferation, metastasis, cell cycle, and apoptosis.
- To determine if miR-107-5p directly targets EGFR and to evaluate its therapeutic potential in NSCLC.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) was used to measure miR-107-5p expression in NSCLC tissues and cell lines.
- Functional assays were performed to assess the impact of miR-107-5p on cell proliferation, migration, invasion, cell cycle progression, and apoptosis.
- Bioinformatic analysis and luciferase reporter assays were employed to validate EGFR as a direct target of miR-107-5p.
- In vivo studies using animal models were conducted to evaluate the effect of miR-107-5p on tumor growth.
Main Results:
- miR-107-5p expression was found to be significantly downregulated in NSCLC tissues and cell lines compared to normal controls.
- Overexpression of miR-107-5p suppressed NSCLC cell proliferation, inhibited metastasis, impeded cell cycle progression, and promoted apoptosis.
- EGFR was identified as a direct target of miR-107-5p, and its expression was inversely correlated with miR-107-5p levels.
- In vivo experiments demonstrated that miR-107-5p administration inhibited tumor growth in NSCLC models.
Conclusions:
- miR-107-5p acts as a tumor suppressor in NSCLC by directly targeting and inhibiting the expression of EGFR.
- Restoration of miR-107-5p levels can impede NSCLC progression and inhibit tumor growth.
- miR-107-5p represents a promising novel therapeutic target for the treatment of lung cancer.
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