Erratum: Ras-related protein Rap2c promotes the migration and invasion of human osteosarcoma cells.

[This corrects the article DOI: 10.3892/ol.2018.7987.].

Rap2c as a Novel Biomarker for Predicting Poor Prognosis in Glioma.

OBJECTIVE: Rap2c is a member of the Ras superfamily that has been implicated in various types of cancers. However, its role in glioma remains elusive. This study aimed to elucidate the role of Rap2c in glioma and its specific molecular mechanism. METHODS: We determined the expression of Rap2c in glioma tissues by Western blotting and immunohistochemistry (IHC) assays. The proliferation and apoptosis of cells were explored using CCK-8 and flow cytometry assay, whereas the migration and invasion of glioma cells were determined using transwell assay. The potential mechanism of Rap2c in the migration of glioma cell lines was investigated through Western blotting analysis and transwell assay. BALB/c nude mice were used to establish tumor models to test the effect of Rap2c on cancer metastasis in vivo. RESULTS: Our data showed that the protein expression of Rap2c was significantly up-regulated in glioma tissues compared with normal brain tissues, and Rap2c overexpression negatively correlated with 5-year overall survival rate. However, there was no correlation between Rap2c expression and clinicopathological parameters of glioma patients. Overexpression of Rap2c promoted the migration and invasion abilities of glioma cells but had no significant effect on the proliferation of glioma cells. Western blotting analysis revealed that Rap2c overexpression increased the phosphorylation level of extracellular signal-related kinase1/2 (ERK1/2), and this effect was abolished with U0126, a selective MEK inhibitor. Furthermore, overexpression of Rap2c induced lung metastasis of glioma cells in xenograft models. CONCLUSION: These findings indicate that high Rap2c expression predicts poor prognosis in glioma. Rap2c-mediated ERK1/2 phosphorylation initiates EMT cascade and promotes migration and invasion of glioma cells. Thus, targeting Rap2c and ERK signaling pathway could be a novel treatment modality for glioma.

Ras-related protein Rap2c promotes the migration and invasion of human osteosarcoma cells.

Ras-related protein (Rap)2a and Rap2b are members of the GTP-binding protein family, and serve an important function in tumor progression. However, the associations between Rap2c and cancer cell functions have not yet been reported. Osteosarcoma is a type of bone cancer; its high degree of invasion is considered to be a major treatment challenge. The present study first investigated the biological role of Rap2c in human osteosarcoma cells and investigated the underlying mechanism of Rap2c on osteosarcoma cell migration and invasion. The results of the present study demonstrated that Rap2c overexpression promoted the migratory and invasive ability of cancer cells, and increased the activity of matrix metalloproteinase-2 (MMP2). Correspondingly, the knockdown of Rap2c inhibited tumor cell migration and invasion, whereas alterations to Rap2c had no effect on osteosarcoma cell proliferation or rate of apoptosis. Furthermore, Rap2c overexpression may decrease the protein level of tissue inhibitor of metalloproteinases 2 and increase the phosphorylation level of protein kinase B (Akt). Collectively, these results indicated that Rap2c has a key function in tumor migration and invasion, and the Akt signaling pathway may be involved in Rap2c-induced MMP2 expression.

Rap2a serves as a potential prognostic indicator of renal cell carcinoma and promotes its migration and invasion through up-regulating p-Akt.

Rap2a, a member of the small GTPase superfamily, belongs to Ras superfamily, and its function in cancer progression is still poorly understood. Our previous study indicated that the ectopic expression of Rap2a enhanced the migration and invasion ability of lung cancer cells. However, its expression and molecular mechanism on renal cell carcinoma (RCC) have not been characterized. This study explored the clinical significance and biological function of Rap2a in human RCC. The clinical relevance of Rap2a in RCC was evaluated by immunohistochemical staining using tissue microarray. Our data showed that Rap2a expression was dramatically increased in RCC tissues compared with normal renal tissues. The ectopic expression of Rap2a enhanced the migration and invasive ability of cancer cells. In contrast, downregulation of Rap2a inhibited cell invasion. Rap2a had no effect on the proliferation of RCC cell lines. Meanwhile, Rap2a can regulate the phosphorylation level of Akt in vitro. In vivo studies also showed that Rap2a positively regulated metastasis of renal cancer cells and the expression of p-Akt. These findings indicate that Rap2a promotes RCC metastasis and may serve as a candidate RCC prognostic marker and a potential therapeutic target.