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Updated: Apr 7, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MiR-449c inhibits gastric carcinoma growth
Zhiming Wu1, Huangen Wang1, Sunyang Fang1
1Department of Surgery, Shaoxing Hospital of China Medical University, 1 Huayu Road, Shaoxing 312030, China.
Aims:
Gastric carcinoma (GC) is among the leading causes of cancer-related deaths in China. Growing evidence indicates that dysregulation of miRNAs contributes to GC development. Although it has been shown that miR-449c acts as a tumor suppressor in lung cancer, the role of miR-449c in GC remains unclear.
Main Methods:
Here, we analyzed miR-449c levels in GC tissues and cell lines by RT-qPCR. We also overexpressed and inhibited miR-449c by transfecting miRNA mimics and antisense oligonucleotides (ASO), respectively. Cell growth was analyzed by MTT assay, and cell apoptosis was evaluated by FACS analysis. MiR-449c target genes were predicted using bioinformatics algorithms and confirmed by a dual luciferase reporter assay.
Key Findings:
We detected lower miR-449c levels in GC tissues; the low miR-449c levels correlated with low survival rate. Overexpression of miR-449c inhibited cell growth and promoted apoptosis, while depletion of miR-449c increased cell growth and suppressed apoptosis. Moreover, the 3' UTR of MET, an oncogene that activates tumor cell growth, appeared to be targeted by miR-449c.
Significance:
Together, we showed that the reduced miR-449c levels in GC tissues promote GC growth, which possibly contributes to the low survival rate of GC patients. Mechanistically, miR-449c may target MET to suppress GC cell growth.
Insights
Reduced miR-449c levels in gastric cancer (GC) tissues correlate with poor survival. This microRNA suppresses GC cell growth and promotes apoptosis, potentially by targeting the MET oncogene.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Gastric carcinoma (GC) is a major cause of cancer mortality in China.
- MicroRNA (miRNA) dysregulation is implicated in GC development.
- The tumor-suppressive role of miR-449c in lung cancer is established, but its function in GC is unknown.
Purpose of the Study:
- To investigate the role of miR-449c in gastric carcinoma.
- To determine the relationship between miR-449c levels and patient survival.
- To elucidate the molecular mechanism of miR-449c in GC progression.
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (RT-qPCR) to measure miR-449c levels in GC tissues and cell lines.
- Transfection with miRNA mimics and antisense oligonucleotides (ASO) to overexpress and inhibit miR-449c.
- Cell proliferation assays (MTT) and apoptosis analysis (FACS).
- Bioinformatic prediction and dual-luciferase reporter assays to identify miR-449c targets.
Main Results:
- Lower miR-449c expression was observed in GC tissues, correlating with reduced patient survival rates.
- Overexpression of miR-449c inhibited GC cell growth and induced apoptosis.
- Inhibition of miR-449c promoted GC cell growth and suppressed apoptosis.
- The MET oncogene was identified as a direct target of miR-449c, with binding occurring at the 3' untranslated region (UTR).
Conclusions:
- Reduced miR-449c levels contribute to GC progression and are associated with poor patient outcomes.
- miR-449c functions as a tumor suppressor in GC, potentially through targeting MET.
- These findings highlight miR-449c as a potential therapeutic target for gastric cancer.
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