Background: Osteosarcoma (OS) is among the most prevalent forms of malignant tumors seen in children and teenagers. Early metastasis is a hallmark of OS, and it is therefore important to find new and more effective treatment targets to improve the survival time of patients with the disease. High mobility group N (HMGNs) is a family of proteins that contributes to the development of a number of different tumors. In particular, HMGN2 was found in our earlier study to be an anti-tumor factor and was seen to impede the metastasis of OS when it was overexpressed. This study aims to further investigate the potential of HMGN2 in anti-tumor treatment.
Methods: We overexpressed HMGN2 in 293FT cells via transfection with recombinant lentiviruses and purified HMGN2 protein with flag tags to treat OS cell lines. The cellular location of exogenous HMGN2 was detected by immunocytochemistry, and wound healing and transwell assays were used to study differences in the rates of migration and invasion of cells between each group.
Results: We found that exogenous HMGN2 enters OS cells in a concentration-dependent manner and inhibits the migration and invasion of OS cells, and exogenous HMGN2 regulates the expression of matrix metalloproteinase 2 (MMP2) and MMP9 in OS cells.
Conclusions: Our results demonstrated that exogenous HMGN2 plays a role in inhibiting OS metastasis, which could act as a basis for new ideas for future anti-tumor therapy research.
Keywords: HMGN2; antitumor; exogenous; metastasis; osteosarcoma (OS).
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