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Updated: May 19, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
[Suppression of Aurora-A by RNA interference inhibits laryngeal cancer Hep-2 cell growth]
Hao Zhang1, Xue-hua Chen, Chang-ping Cai
1Department of Otorhinolaryngology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200025, China.
Objective:
To investigate the effects of knockdown of Aurora-A by RNA interference on laryngeal cancer Hep-2 cell growth in vitro and in vivo.
Methods:
A plasmid containing siRNA against Aurora-A was constructed and transfected into human laryngeal cancer cell line Hep-2. Measurements included the CCK-8 assay for viability and proliferation, Transwell assay for invasion, colony formation assay for cell anchorage-independent growth. Western blot and immunohistochemistry assay for protein expression. Tumorigenicity was observed in vivo.
Results:
In Hep-2 cells transfected by Aurora-A siRNA (designated as siRNA-3), protein expression of Aurora-A was suppressed by 52%. In CCK-8 assay, absorbance value of siRNA-3 cells (3.268 ± 0.106, (x(-) ± s)) was lower than that of Hep-2 cells (3.722 ± 0.152, F = 17.634, P < 0.001). In Transwell assay, the average invasive cells per field in siRNA-3 cells (110.0 ± 18.0) was less than that in Hep-2 cells (236.0 ± 26.0, F = 26.462, P < 0.01). In colony formation assay, the average colony number of siRNA-3 cells (31.0 ± 6.6) was lower than that of Hep-2 cells (104.0 ± 14.0). The average tumor size in siRNA-3 group was (127.77 ± 174.83) mm(3), which was less than Hep-2 cell group (837.26 ± 101.80) mm(3), (F = 28.187, P < 0.001). Silencing of Aurora-A decreased the expression of focal adhesion kinase (FAK) and matrix metalloproteinase-2 (MMP-2), key regulators in cell adhesion and invasion.
Conclusions:
The knockdown of Aurora-A inhibits the growth and invasiveness of Hep-2 cells in vitro and in vivo, which may be a promising therapeutic strategy for LSCC.
Insights
Knocking down Aurora-A kinase using RNA interference significantly inhibits laryngeal cancer Hep-2 cell growth and invasion. This suggests Aurora-A is a potential therapeutic target for laryngeal squamous cell carcinoma (LSCC).
Area of Science:
- Molecular Biology
- Oncology
- Cell Biology
Background:
- Aurora-A kinase is implicated in cell proliferation and cancer progression.
- Understanding Aurora-A's role in laryngeal cancer is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the impact of Aurora-A knockdown via RNA interference on laryngeal cancer Hep-2 cell behavior.
- To evaluate the in vitro and in vivo effects of Aurora-A inhibition on tumor growth and invasiveness.
Main Methods:
- Constructed a plasmid with small interfering RNA (siRNA) targeting Aurora-A.
- Transfected human laryngeal cancer Hep-2 cells with the siRNA plasmid.
- Assessed cell viability, proliferation (CCK-8 assay), invasion (Transwell assay), anchorage-independent growth (colony formation assay), and protein expression (Western blot, immunohistochemistry). Evaluated tumorigenicity in vivo.
Main Results:
- Aurora-A protein expression was reduced by 52% in Hep-2 cells transfected with Aurora-A siRNA.
- Knockdown of Aurora-A significantly decreased Hep-2 cell viability, proliferation, invasion, and anchorage-independent growth.
- Tumor growth in vivo was significantly inhibited in the Aurora-A knockdown group, with reduced expression of FAK and MMP-2.
Conclusions:
- Silencing Aurora-A effectively inhibits the growth and invasiveness of laryngeal cancer Hep-2 cells.
- Aurora-A represents a promising therapeutic target for laryngeal squamous cell carcinoma (LSCC).
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