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Updated: Feb 7, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
miR-5590-3p inhibited tumor growth in gastric cancer by targeting DDX5/AKT/m-TOR pathway
Nan Wu1, Yuying Han1, Haiming Liu2
1Laboratory of Tissue Engineering, Faculty of Life Science, Northwest University, 229 Tai Bai North Road, Xi'an, Shaanxi, 710069, China.
Abstract:
Recent evidence suggests that microRNAs play important roles in the negative post-transcriptional regulators with altered expression levels found in gastric cancer (GC). Therefore, we employed explore the anti-cancer miRNA and the potential mechanisms by which miRNAs modulate GC progression. We have predicted GC miRNA expression data sets in TargetScan. miR-5590-3p is higher in adjacent nonmalignant tissue than in cancer tissue in 42 pairs of GC tissues. Functional assays, CCK-8 and colony formation assay, were used to determine the Anti-cancer role of miR-5590-3p in human GC progression. In addition, Ago2-based RIP and dual-luciferase reporter assay were conducted to study the miR-5590-3p as a direct target of DDX5. Next, Xenograft nude mouse models were used to determine the role of miR-5590-3p in GC tumorigenicity in vivo. Upregulation of miR-5590-3p suppressed GC cell proliferation, whereas downregulation of miR-5590-3p promoted GC proliferation in vitro. Furthermore, we identified DDX5 as a direct target of miR-5590-3p, and that the biological function of miR-5590-3p during GC progression in vitro and in vivo is through the DDX5/AKT/m-TOR pathway and downstream cyclinD1 and CDK2 expression. Finally, we confirmed the effect of miR-5590-3p directly targeting DDX5 on the development of gastric cancer through salvage experiments in vivo and in vitro.
Insights
MicroRNA-5590-3p acts as an anti-cancer agent in gastric cancer (GC). Upregulating this microRNA suppresses tumor growth by targeting DDX5, offering a potential therapeutic strategy for GC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are key post-transcriptional regulators implicated in gastric cancer (GC) pathogenesis.
- Altered miRNA expression is frequently observed in GC, highlighting their potential as diagnostic and therapeutic targets.
Purpose of the Study:
- To investigate the anti-cancer role of miR-5590-3p in gastric cancer.
- To elucidate the molecular mechanisms underlying miR-5590-3p's function in GC progression.
- To identify direct targets and signaling pathways modulated by miR-5590-3p.
Main Methods:
- Bioinformatic prediction of miRNA expression in GC using TargetScan.
- In vitro functional assays (CCK-8, colony formation) to assess cell proliferation.
- Ago2-based RIP and dual-luciferase reporter assays to confirm direct target interactions.
- In vivo studies using xenograft nude mouse models to evaluate tumorigenicity.
Main Results:
- miR-5590-3p was found to be downregulated in GC tissues compared to adjacent non-malignant tissues.
- Upregulation of miR-5590-3p suppressed GC cell proliferation in vitro, while downregulation promoted it.
- DDX5 was identified as a direct target of miR-5590-3p.
- miR-5590-3p exerts its anti-cancer effects through the DDX5/AKT/m-TOR pathway, affecting downstream cyclinD1 and CDK2 expression.
Conclusions:
- miR-5590-3p functions as a tumor suppressor in gastric cancer.
- Targeting DDX5 by miR-5590-3p inhibits GC progression both in vitro and in vivo.
- miR-5590-3p represents a potential therapeutic target for gastric cancer treatment.
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