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Updated: Dec 13, 2025
In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MicroRNA-126-5p suppresses cell proliferation, invasion and migration by targeting EGFR in liver cancer
Yanping Zhao1, Lei Ye1, Yaping Yu1
1The First Affiliated Hospital of Zhejiang University of Traditional Chinese Medicine, NO.1 Building, Yunbin Bay, Jianggan District, Hangzhou 310000, Zhejiang, China.
Background:
The expression status and potential mechanistic involvement of microRNA (miR)-126-5p in hepatocellular carcinoma (HCC) are still elusive currently. Here we set out to address this issue both in cell lines and in patients' tissues.
Methods:
The relative expression levels of endogenous miR-126-5p and epidermal growth factor receptor (EGFR) were quantified by real-time polymerase chain reaction. Cell viability and proliferation were measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and clonogenic assays, respectively. Cell invasive and migrative capacities were determined by transwell and wound healing assays, respectively. The regulatory action of miR-126-5p on EGFR was interrogated by luciferase reporter assay. Translational level of EGFR was analyzed by Western blotting.
Results:
MiR-126-5p was significantly down-regulated in both HCC patients' tissues and cell lines. Forced expression of miR-126-5p greatly compromised cell viability, proliferation, invasion and migration, while miR-126-5p-specific inhibitor promoted these oncogenic phenotypes. MiR-126-5p mimics inhibited endogenous expression of EGFR and suppressed EGFR 3'-untranslated region-fused luciferase activity. Co-expression of EGFR in miR-126-5p-proficient cells completely restored cell migrative and invasive capacities, while co-transfection with EGFR siRNA significantly inhibited miR-126-5p inhibitor-induced cell invasion and migration.
Conclusion:
MiR-126-5p was aberrantly decreased in HCC and subsequently relieved the suppression on EGFR expression, which consequently contributed to the tumor biology of HCC.
Insights
MicroRNA-126-5p is down-regulated in hepatocellular carcinoma (HCC), promoting tumor growth by increasing epidermal growth factor receptor (EGFR) expression. Restoring miR-126-5p levels inhibits HCC progression.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- The role of microRNA (miR)-126-5p in hepatocellular carcinoma (HCC) remains unclear.
- Investigating miR-126-5p's expression and function is crucial for understanding HCC pathogenesis.
Purpose of the Study:
- To elucidate the expression status and mechanistic role of miR-126-5p in HCC.
- To determine the relationship between miR-126-5p and epidermal growth factor receptor (EGFR) in HCC.
Main Methods:
- Quantified miR-126-5p and EGFR expression using real-time PCR.
- Assessed cell viability, proliferation, invasion, and migration using established assays.
- Investigated miR-126-5p's regulatory effect on EGFR via luciferase reporter and Western blot analyses.
Main Results:
- miR-126-5p was significantly downregulated in HCC tissues and cell lines.
- Overexpression of miR-126-5p suppressed HCC cell viability, proliferation, invasion, and migration.
- miR-126-5p directly targeted and inhibited EGFR expression, impacting HCC phenotypes.
Conclusions:
- Aberrant downregulation of miR-126-5p in HCC relieves suppression on EGFR.
- This leads to increased EGFR expression, contributing to the tumor biology of HCC.
- miR-126-5p acts as a tumor suppressor in HCC by targeting EGFR.
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