RhoB Overexpression Inhibits the Progression of Osteosarcoma and Its Clinical Significance

Abstract

Purpose: Osteosarcoma (OS) is a serious malignant tumor in orthopedics, which seriously endangers the life and health of adolescents. Ras homolog family member B (RhoB) is known to function as an anti-oncogene in a series of cancers, including OS. This study focused on the function of RhoB on cell growth and apoptosis in OS. Methods: Immunohistochemistry (IHC), Western blot and Real-time quantitative polymerase chain reaction (RT-qPCR) assay were performed to examine RhoB level in OS tissues and cells (HOS, MG63, Saos-2). The effect of RhoB overexpression on the proliferation ability of MG63 and HOS cells was verified by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and plate clone formation assay. The impact of RhoB overexpression on OS cell apoptosis was verified by flow cytometry (FCM) and the detection of apoptosis-related proteins. The function of RhoB overexpression on lung metastasis and tumor growth in vivo was studied by xenograft experiments. In addition, the regulation of RhoB on the PI3K/AKT pathway in OS was investigated by Western blot assay. Results: The reduced expression of RhoB was verified in 62 OS tissues and 3 OS cell lines (HOS, MG63, Saos-2). The enhanced expression of RhoB notably impaired cell proliferation but facilitated cell apoptosis in MG63 and HOS cells. Furthermore, RhoB overexpression blocked xenograft tumour growth and lung metastasis in vivo. Additionally, the phosphorylation of AKT and PI3K was decreased by RhoB overexpression but elevated by RhoB knockdown. Conclusions: Altogether, our findings displayed that enhanced expression of RhoB suppressed OS cell progression by inactivating the PI3K/AKT pathway.