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Updated: Mar 9, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MicroRNA-613 suppresses proliferation, migration and invasion of osteosarcoma by targeting c-MET
Xinyu Li1, Xufang Sun1, Jing Wu2
1Department of Anesthesiology, The Second Hospital, Jilin University Changchun 130041, China.
Abstract:
MicroRNA-613 (miR-613) has been reported to play an important role in the pathogenesis of multiple cancers by negatively regulating gene expression at posttranscriptional level. However, the biological role of miR-613 in osteosarcoma (OS) remained unclear. In this study, we aimed to determine the expression and biological roles of miR-613 in OS. We found that miR-613 was significantly downregulated in OS tissues and cell lines, and that decreased miR-613 expression was correlated negatively with advanced TNM stage and lymph node metastasis. Overexpression of miR-613 in OS cells significantly suppressed the proliferation and colony formation by regulating cell arrest at G0/G1 phase, and impaired the migration and invasive abilities of OS cells, followed by suppression of the epithelial mesenchymal transition (EMT). Bioinformatic and luciferase reporter analysis identified cellular-mesenchymal to epithelial transition factor (c-MET, also named as MET) as a direct target of miR-613. Overexpression of miR-613 significantly inhibited the c-MET expression and its downstream PI3k/Akt/mTOR signaling pathway in OS cells. In OS clinical samples, there was a significant inverse correlation between miR-613 and c-MET mRNA expression. Rescue experiments showed that overexpression of c-MET partially prevented miR-613-induced suppression of OS cell proliferation, colony formation, migration and invasion. In conclusion, we provide first evidence for the suppressive activity of miR-613 by repressing c-MET, suggesting that miR-613 might be a potential therapeutic strategy for OS.
Insights
MicroRNA-613 (miR-613) is downregulated in osteosarcoma (OS), suppressing cancer cell growth and metastasis by targeting c-MET. This suggests miR-613 as a potential therapeutic strategy for OS patients.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- MicroRNA-613 (miR-613) regulates gene expression posttranscriptionally and is implicated in various cancers.
- The specific role of miR-613 in osteosarcoma (OS) pathogenesis was previously unclear.
Purpose of the Study:
- To investigate the expression patterns and functional significance of miR-613 in osteosarcoma.
- To identify the molecular targets and signaling pathways regulated by miR-613 in OS.
Main Methods:
- Quantitative real-time PCR to assess miR-613 expression in OS tissues and cell lines.
- Cell proliferation, colony formation, migration, and invasion assays to evaluate miR-613 function.
- Bioinformatic analysis and luciferase reporter assays to identify miR-613 targets.
- Western blotting and rescue experiments to validate target interaction and pathway modulation.
Main Results:
- miR-613 was significantly downregulated in OS tissues and cell lines, inversely correlated with advanced TNM stage and lymph node metastasis.
- Overexpression of miR-613 suppressed OS cell proliferation, colony formation, migration, and invasion, inhibiting epithelial-mesenchymal transition (EMT).
- Cellular-mesenchymal to epithelial transition factor (c-MET) was identified as a direct target of miR-613; miR-613 inhibited c-MET expression and the PI3K/Akt/mTOR pathway. Overexpression of c-MET partially rescued miR-613's suppressive effects.
Conclusions:
- miR-613 functions as a tumor suppressor in osteosarcoma by targeting c-MET and inhibiting downstream signaling pathways.
- Restoring miR-613 expression may represent a novel therapeutic strategy for osteosarcoma.
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