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Updated: Dec 26, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MiR-26a/miR-26b represses tongue squamous cell carcinoma progression by targeting PAK1
Zhenxing Wei1, Kunpeng Chang1, Chongsheng Fan1
1Department of Otorhinolaryngology-Head and Neck Surgery, The Luoyang Central Hospital Affiliated to Zhengzhou University, No. 288 Middle Zhongzhou Road, Xigong District, Luoyang, 471000 Henan China.
Background:
Tongue squamous cell carcinoma (TSCC) is the most common oral malignancy. Previous studies found that microRNA (miR)-26a and miR-26b were downregulated in TSCC tissues. The current study was designed to explore the effects of miR-26a/miR-26b on TSCC progression and the potential mechanism.
Methods:
Expression of miR-26a, miR-26b and p21 Activated Kinase 1 (PAK1) in TSCC tissues and cell lines was detected by reverse transcription- quantitative polymerase chain reaction (RT-qPCR). Flow cytometry analysis was performed to examine cell cycle and apoptosis. Transwell assay was conducted to evaluate the migrated and invasive abilities of SCC4 and Cal27 cells. In addition, western blot assay was employed to analyze the protein level. Glucose assay kit and lactate assay kit were utilized to analyze glycolysis. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were applied to explore the relationship between miR-26a/miR-26b and PAK1. Xenograft tumor model was constructed to explore the role of miR-26a/miR-26b in vivo.
Results:
Both miR-26a and miR-26b were underexpressed, while PAK1 was highly enriched in TSCC. Overexpression of miR-26a and miR-26b inhibited TSCC cell cycle, migration invasion and glycolysis, while promoted cell apoptosis. Both miR-26a and miR-26b directly targeted and negatively regulated PAK1 expression. Introduction of PAK1 partially reversed miR-26a/miR-26b upregulation-mediated cellular behaviors in TSCC cells. Gain of miR-26a/miR-26b blocked TSCC tumor growth in vivo.
Conclusion:
MiR-26a/miR-26b repressed TSCC progression via targeting PAK1 in vitro and in vivo, which enriched our understanding about TSCC development and provided new insights into the its treatment.
Insights
MicroRNA (miR)-26a and miR-26b suppress tongue squamous cell carcinoma (TSCC) progression by targeting p21 Activated Kinase 1 (PAK1). Restoring these microRNAs inhibits tumor growth, offering new therapeutic strategies for TSCC.
Area of Science:
- Molecular Oncology
- Cancer Biology
- MicroRNA Therapeutics
Background:
- Tongue squamous cell carcinoma (TSCC) is a prevalent oral malignancy.
- Previous research indicated reduced expression of microRNA (miR)-26a and miR-26b in TSCC tissues.
Purpose of the Study:
- To investigate the impact of miR-26a and miR-26b on TSCC progression.
- To elucidate the underlying molecular mechanisms involving p21 Activated Kinase 1 (PAK1).
Main Methods:
- Quantitative polymerase chain reaction (RT-qPCR) and western blotting to assess miR-26a, miR-26b, and PAK1 expression.
- Flow cytometry for cell cycle and apoptosis analysis.
- Transwell assays for cell migration and invasion.
- Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays to confirm miR-26a/miR-26b and PAK1 interaction.
- In vivo studies using a xenograft tumor model.
Main Results:
- miR-26a and miR-26b were underexpressed, while PAK1 was highly expressed in TSCC.
- Overexpression of miR-26a/miR-26b suppressed TSCC cell proliferation, migration, invasion, and glycolysis, while enhancing apoptosis.
- miR-26a/miR-26b directly targeted and downregulated PAK1; PAK1 introduction partially reversed these effects.
- Restoration of miR-26a/miR-26b inhibited TSCC tumor growth in vivo.
Conclusions:
- miR-26a and miR-26b act as tumor suppressors in TSCC by targeting PAK1.
- These findings enhance the understanding of TSCC pathogenesis.
- miR-26a/miR-26b represent potential therapeutic targets for TSCC treatment.
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