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Updated: Nov 20, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
miRNA-128 modulates bone neoplasms cells proliferation and migration through the WNT/β-catenin and EMT signal
Yang Li1, Xiaotao Long1, Ji Wang1
1Department of Orthopedics, Chongqing General Hospital, University of the Chinese Academy of Sciences, No. 312 Zhongshanyi Road, Yuzhong District, Chongqing, 400013, China.
Background:
Bone neoplasms present poor prognosis due to recurrence and metastasis. Although the role microRNAs (miRNAs) in inhibiting growth and metastasis of bone neoplasms has been investigated, the underlying potential molecular mechanisms mediated by miRNA-128 (miR-218) for the invasiveness of bone neoplasms cells are still not completely understood. The purpose of this study was to identify the regulatory mechanisms of miR-218 in bone neoplasms cells.
Methods:
Western blotting, quantitative reverse transcription-polymerase chain reaction (qRT-PCR), Counting Kit-8 assay, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, luciferase activity assay immunofluorescence, and immunohistochemistry were used to analyze the regulatory effects of miR-218 on bone neoplasms cells.
Results:
Here, the results showed that transfection of miR-128 suppressed bone neoplasms cells proliferation, migration, and invasion. Genetic knockdown of miR-128 in bone neoplasms cells suppressed the activation of the Wnt/β-catenin and epithelial-mesenchymal transition (EMT) signaling pathways. Activation of Wnt or EMT blocked miR-128-inhibited cells proliferation and migration in bone neoplasms cells. Exogenously introduced miR-128 markedly inhibited tumor regeneration in bone neoplasms xenograft models.
Conclusions:
These results define a tumor-regulated function for miR-128 in bone neoplasms by down-regulation of the Wnt/β-catenin and EMT signal pathways, which provided a potential target for bone neoplasms gene therapy.
Insights
MicroRNA-128 (miR-128) suppresses bone neoplasm growth and metastasis by inhibiting Wnt/β-catenin and epithelial-mesenchymal transition (EMT) pathways. This finding offers a potential gene therapy target for bone neoplasms.
Area of Science:
- Oncology
- Molecular Biology
- Gene Therapy
Background:
- Bone neoplasms are aggressive with high recurrence and metastasis rates.
- MicroRNAs (miRNAs) show potential in inhibiting bone neoplasm progression.
- The specific role of microRNA-128 (miR-128) in bone neoplasm invasiveness requires further elucidation.
Purpose of the Study:
- To investigate the regulatory mechanisms of miR-128 in bone neoplasm cells.
- To understand how miR-128 influences cancer cell proliferation, migration, and invasion.
Main Methods:
- Western blotting and qRT-PCR to analyze protein and RNA levels.
- Cell proliferation, migration, and invasion assays (e.g., CCK-8, TUNEL).
- Luciferase assays, immunofluorescence, and immunohistochemistry to assess pathway activation.
Main Results:
- miR-128 transfection suppressed bone neoplasm cell proliferation, migration, and invasion.
- miR-128 knockdown activated Wnt/β-catenin and epithelial-mesenchymal transition (EMT) pathways.
- Wnt/EMT pathway activation counteracted miR-128's inhibitory effects.
- Exogenous miR-128 significantly inhibited tumor growth in xenograft models.
Conclusions:
- miR-128 down-regulates Wnt/β-catenin and EMT signaling in bone neoplasms.
- miR-128 exhibits tumor-suppressive functions in bone neoplasms.
- Targeting miR-128 presents a potential strategy for bone neoplasm gene therapy.
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