MiR-155 Promotes the Growth of Osteosarcoma in a HBP1-dependent Mechanism
Overview
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Osteosarcoma (OS) is a type of malignant tumor arising from soft-tissues of bone and displays poor prognosis in most cases. However, the molecular mechanism by which OS initiates and progresses is still not completely elucidated. miR-155 has been shown to be overexpressed in OS specimen and cell lines. Our study is intended to explore the role of miR-155 in OS etiology. The data confirmed that miR-155 abundance is higher in OS samples than non-cancerous bone tissue. Inhibition of miR-155 suppressed the proliferation of OS cells and cell cycle progression in vitro, and the growth of OS xenografts in vivo. Wnt pathway was suppressed in OS cells by miR-155 inhibitors. HMG-box transcription factor 1 (HBP1), a strong Wnt pathway suppressor, was found to be a target of miR-155. Restoration of HBP1 abolished the effect of miR-155 on OS cells. Finally, miR-155 levels in OS tissues and serum are both inversely associated with the survival of OS patients. Collectively, miR-155 was identified to be among the list of OS-related oncogenic miRNAs, and HBP1-mediated Wnt signaling is involved with the role of miR-155 in OS progression.
Huang W, Hong Q, Wang H, Zhu Z, Gong S eNeuro. 2025; 12(2).
PMID: 39788733 PMC: 11842039. DOI: 10.1523/ENEURO.0347-24.2024.
The role of miR-155 in cardiovascular diseases: Potential diagnostic and therapeutic targets.
Zhang R, Wang W, Li J, Li R, Zhang J, Wu Y Int J Cardiol Cardiovasc Risk Prev. 2025; 24:200355.
PMID: 39760132 PMC: 11699627. DOI: 10.1016/j.ijcrp.2024.200355.
Research Progress of Exosome-Loaded miRNA in Osteosarcoma.
Yao P, Lu Y, Cai Z, Yu T, Kang Y, Zhang Y Cancer Control. 2022; 29:10732748221076683.
PMID: 35179996 PMC: 8859673. DOI: 10.1177/10732748221076683.
Wei Y, Lu W, Yu Y, Zhai Y, Guo H, Yang S Oncogene. 2021; 40(19):3434-3448.
PMID: 33888868 DOI: 10.1038/s41388-021-01775-9.
Li N, Ouyang Y, Xu X, Yuan Z, Liu C, Zhu Z J Cell Mol Med. 2021; 25(10):4765-4775.
PMID: 33769664 PMC: 8107084. DOI: 10.1111/jcmm.16445.