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Updated: Apr 11, 2026

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
Published on: April 12, 2019
Overexpression of miR-100 inhibits growth of osteosarcoma through FGFR3
Yunlong Bi1, Yu Jing2, Yang Cao3
1Department of Orthopedics, The First Affiliated Hospital of Liaoning Medical University, 5-2, Renmin Street, Jinzhou, 121000, China.
Abstract:
Osteosarcoma (OS) is a prevalent, fast growing cancer. Identification of molecular regulation of OS growth may result in development of a novel therapy. Previous studies have highlighted a role of microRNAs (miRNAs) in the regulation of the carcinogenesis of OS, whereas the underlying mechanisms are not completely understood. Moreover, a role of miR-100 in the growth control of OS is not clear. Here we reported significantly higher levels of fibroblast growth factor receptor 3 (FGFR3) and significantly lower levels of miR-100 in the OS specimen, compared to those in the paired normal bone tissues. Bioinformatics analysis and luciferase reporter assay suggest that miR-100 binds to the 3'UTR of FGFR3 mRNA to prevent its translation. To prove it, we modified miR-100 levels in OS cells. We found that overexpression of miR-100 in OS cells decreased FGFR3 protein levels, whereas inhibition of miR-100 increased FGFR3 protein levels, without affecting FGFR3 transcripts. Moreover, overexpression of miR-100 suppressed the OS growth in vitro and in vivo, while inhibition of miR-100 significantly increased OS growth. Taken together, our data demonstrate that miR-100 may inhibit the growth of OS through FGFR3.
Insights
MicroRNA-100 (miR-100) inhibits osteosarcoma (OS) growth by targeting fibroblast growth factor receptor 3 (FGFR3). Lower miR-100 and higher FGFR3 levels were observed in OS tissues, suggesting a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Osteosarcoma (OS) is a rapidly growing bone cancer with complex molecular underpinnings.
- MicroRNAs (miRNAs) are implicated in cancer development, but their specific roles in OS, particularly miR-100, remain unclear.
- Understanding the molecular mechanisms of OS growth is crucial for developing novel therapeutic strategies.
Purpose of the Study:
- To investigate the role of miR-100 in the regulation of osteosarcoma cell growth.
- To identify the molecular targets of miR-100 involved in osteosarcoma pathogenesis.
- To explore the potential of targeting the miR-100/FGFR3 axis for osteosarcoma therapy.
Main Methods:
- Comparative analysis of miR-100 and fibroblast growth factor receptor 3 (FGFR3) expression in OS and normal bone tissues.
- Bioinformatics analysis and luciferase reporter assays to confirm the interaction between miR-100 and FGFR3 mRNA.
- In vitro and in vivo experiments involving modulation of miR-100 levels in OS cells to assess effects on FGFR3 expression and tumor growth.
Main Results:
- Significantly lower levels of miR-100 and higher levels of FGFR3 were detected in osteosarcoma tissues compared to normal bone.
- miR-100 directly binds to the 3'UTR of FGFR3 mRNA, inhibiting its translation into protein.
- Overexpression of miR-100 suppressed OS cell proliferation and tumor growth in vitro and in vivo, while miR-100 inhibition promoted growth.
Conclusions:
- The study identifies a novel inhibitory role for miR-100 in osteosarcoma progression.
- The miR-100/FGFR3 signaling pathway is a key regulator of osteosarcoma cell growth.
- Targeting miR-100 or its downstream effector FGFR3 presents a promising therapeutic avenue for osteosarcoma treatment.
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