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A Preclinical Mouse Model of Osteosarcoma to Define the Extracellular Vesicle-mediated Communication Between Tumor and Mesenchymal Stem Cells
Published on: May 6, 2018
Let-7g reverses malignant phenotype of osteosarcoma cells by targeting Aurora-B
Jia Ming Liu1, Xin Hua Long1, Guo Mei Zhang2
1Department of Orthopedics, The First Affiliated Hospital of Nanchang University Jiangxi, China.
Abstract:
Accumulating studies revealed that the expression levels of several miRNAs are up or down-regulated in osteosarcoma (OS). The aim of this study was to investigate the functional significance and molecular of the let-7g in OS cells. The expression levels of let-7g was significantly down-regulated in OS cell lines U2-OS and HOS cell compared to osteoblast cell lines HOB cell. Moreover, bioinformatic prediction suggested that Aurora-B, which is overexpressed and functions as an oncogene in OS cells, is a putative target gene of let-7g. Using mRNA and protein expression analysis and luciferase assays, we further identified let-7g directly regulated Aurora-B expression in OS cells. Functional investigation revealed both restoration of let-7g and silencing Aurora-B induce cell apoptosis and suppressed cell viability, migratory and invasive ability in OS cells. Finally, we found that silencing Aurora-B in OS cells could partly dampen anti-let-7g mediated tumor promotion. Thus, our findings suggested that let-7g inhibits OS cell malignant phenotype at least partly through targeting Aurora-B. Targeting of let-7g and Aurora-B may be a novel therapeutic strategy for treating OS.
Insights
MicroRNAs let-7g are down-regulated in osteosarcoma (OS), inhibiting cancer cell growth by targeting the oncogene Aurora-B. Restoring let-7g or inhibiting Aurora-B may offer new therapeutic strategies for OS.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Osteosarcoma (OS) exhibits altered microRNA (miRNA) expression profiles.
- let-7g is a miRNA with potential roles in tumor suppression.
- Aurora-B is an oncogene frequently overexpressed in OS.
Purpose of the Study:
- To investigate the functional role of let-7g in OS cells.
- To identify molecular targets of let-7g in OS.
- To explore therapeutic potential of targeting let-7g and Aurora-B in OS.
Main Methods:
- Quantitative real-time PCR to assess let-7g expression.
- Bioinformatic analysis to predict let-7g targets.
- Western blotting and luciferase assays to validate let-7g-Aurora-B interaction.
- Cell viability, apoptosis, migration, and invasion assays to evaluate functional effects.
Main Results:
- let-7g expression was significantly downregulated in OS cell lines (U2-OS, HOS) compared to normal osteoblast cells (HOB).
- Aurora-B was identified as a direct target gene of let-7g in OS cells.
- Restoration of let-7g or silencing of Aurora-B suppressed OS cell viability, migration, and invasion, while inducing apoptosis.
- Silencing Aurora-B partially reversed the tumor-promoting effects of anti-let-7g activity.
Conclusions:
- let-7g functions as a tumor suppressor in osteosarcoma by targeting Aurora-B.
- The let-7g/Aurora-B axis plays a crucial role in regulating OS cell malignancy.
- Targeting let-7g and Aurora-B represents a potential novel therapeutic strategy for osteosarcoma treatment.
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