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Updated: Oct 4, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
miR-1290 inhibits chordoma cell proliferation and invasion by targeting Robo1
Bin Wang1,2, Kai Zhang1, Hao Chen1
1Department of Orthopaedic Surgery, The First Affiliated Hospital of Soochow University, Suzhou 215000, China.
Background:
Chordoma is a low-grade aggressive bone tumor with a high local recurrence. MicroRNAs (miRNAs) have been reported to play crucial roles in the development of chordoma. Our previous study has shown miR-1290 is associated with muscle invasion and the prognosis of chordoma. However, the underlying mechanism of miR-1290 in chordoma remains unclear. In this study, we aimed to explore the function of miR-1290 in the biological behaviors of chordoma.
Methods:
Sixteen sacral chordoma samples and 10 fetal nucleus pulposus specimens were collected for the detection of miR-1290 and Robo1 at the First Affiliated Hospital of Soochow University. Bioinformatic analysis and a luciferase reporter assay was used to verify the interaction between miR-1290 and the target gene robo1 in chordoma. Effects of miR-1290 expression on chordoma cell proliferation and invasion were explored by clone formation and Transwell assay in vitro. The underlying mechanisms of miR-1290 and Robo1 in chordoma cell proliferation and invasion were also explored in the U-CH1 cell line.
Results:
In vitro functional analysis, including clone formation, and Transwell assays indicated overexpression of miR-1290 significantly suppressed chordoma cell proliferation and invasion. Bioinformatic analysis revealed Robo1 as a potential target of miR-1290, and luciferase reporter assays demonstrated the association between miR-1290 and the Robo1 gene in U-CH1 cells. Robo1 was further confirmed to be up-regulated in chordoma tissues by immunohistochemistry (IHC), which is negatively correlated with miR-1290 expression in chordoma tissue. Additionally, we found down-regulation of miR-1290 could induce the expression of Robo1 in chordoma cells, while the elevation of miR-1290 expression could inhibit Robo1 expression in chordoma cells.
Conclusions:
miR-1290 inhibits chordoma cell proliferation and invasion by negatively regulating the Robo1 gene.
Insights
MicroRNA 1290 (miR-1290) suppresses chordoma cell growth and spread. This microRNA (miRNA) inhibits chordoma progression by targeting and downregulating the Robo1 gene.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Chordoma is an aggressive bone tumor with high recurrence rates.
- MicroRNAs (miRNAs) are implicated in chordoma development.
- Previous studies linked miR-1290 to chordoma invasion and prognosis, but mechanisms were unclear.
Purpose of the Study:
- To investigate the functional role of miR-1290 in chordoma biological behaviors.
- To elucidate the underlying molecular mechanisms of miR-1290 in chordoma.
Main Methods:
- Analysis of miR-1290 and Robo1 expression in chordoma tissues and fetal specimens.
- Bioinformatic analysis and luciferase reporter assays to identify miR-1290 targets.
- In vitro assays (clone formation, Transwell) to assess effects on cell proliferation and invasion.
- Immunohistochemistry (IHC) to validate Robo1 expression in chordoma tissues.
Main Results:
- Overexpression of miR-1290 significantly inhibited chordoma cell proliferation and invasion in vitro.
- Robo1 was identified as a direct target of miR-1290.
- Robo1 expression was upregulated in chordoma tissues and negatively correlated with miR-1290 levels.
- miR-1290 directly suppressed Robo1 expression in chordoma cells.
Conclusions:
- miR-1290 acts as a tumor suppressor in chordoma.
- miR-1290 inhibits chordoma cell proliferation and invasion by negatively regulating the Robo1 gene.
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