Related Experiment Video
Updated: Dec 16, 2025

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate
Published on: May 3, 2021
Aurora-B Promotes Osteosarcoma Cell Growth and Metastasis Through Activation of the NPM1/ERK/NF-κβ/MMPs Axis
Honghai Song1,2, Yang Zhou1, Aifen Peng3
1Department of Orthopedic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang 330006, People's Republic of China.
Purpose:
Osteosarcoma (OS) is the most common primary malignant tumor of the bone in young adolescents and children. We explored the underlying mechanism of Aurora-B in promoting OS cell proliferation and metastasis.
Patient And Methods:
Bioinformatics was employed to predict the substrate of Aurora-B. IHC and Western blot were used to confirm the correlation between Aurora-B and NPM1. ERK/NF-κβ pathway-related proteins were detected by Western blot and immunofluorescence (IF). CCK8, wound healing, transwell, and Tunel assays were used to identify the cell proliferation, migration and apoptosis potential. Spontaneous metastasis xenografts were established to confirm the role of Aurora-B and NPM1.
Results:
Aurora-B promotes NPM1 phosphorylation on Ser125. The phosphorylation of NPM1Ser125 induced by Aurora-B activates the ERK/NF-κβ signaling. Further study revealed that Aurora-B promotes proliferation, migration and inhibits apoptosis via phosphorylating NPM1 in vitro and in vivo.
Conclusion:
Aurora-B promotes OS malignancy via phosphorylating NPM1Ser125 and activating ERK/NF-κβ signaling.
Related Concept Videos
PI3K/mTOR/AKT Signaling Pathway
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Abnormal Proliferation
MAPK Signaling Cascades
Mitogens and the Cell Cycle

