ArticleJournal of orthopaedic surgery and research2021
miRNA-128 modulates bone neoplasms cells proliferation and migration through the WNT/β-catenin and EMT signal pathways.
Article in Journal of orthopaedic surgery and research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Tumor cell plasticity in targeted therapy-induced resistance: mechanisms and new strategies.Signal transduction and targeted therapy · 2023Review
- Newly Released Advances in the Molecular Mechanisms of Osseous Metastasis and Potential Therapeutic Strategies.The archives of bone and joint surgery · 2022Review
- lncRNA MALAT1 participates in metformin inhibiting the proliferation of breast cancer cell.Journal of cellular and molecular medicine · 2021Article
- Tumor Cell-Derived Exosomal miR-770 Inhibits M2 Macrophage PolarizationFrontiers in cell and developmental biology · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundBone 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.
methodsWestern 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.
resultsHere, 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.
conclusionsThese 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.
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