Glioma represents a disparate group of tumors characterized by high invasion ability, and therefore it is of clinical significance to identify molecular markers and therapeutic targets for better clinical management. Previously, metastasis-associated protein family (MTA) is considered to promote tumor cell invasion and metastasis of human malignancies. Recently, the newly identified MTA3 has been shown to play conflicting roles in human malignancies, while the expression pattern and potential clinical significance of MTA3 in human glioma have not been addressed yet. In the present study, we investigated the protein expression of MTA3 by immunohistochemistry assay and analyzed its association with glioma prognosis in 186 cases of patients. Results showed that MTA3 expression was decreased in glioma compared with that in normal brain (P < 0.05). In addition, tumors with high MTA3 expression were more likely to be of low WHO grade (P = 0.005) and reserve of body function (P = 0.014). Survival analysis showed that decreased MTA3 expression was independently associated with unfavorable overall survival of patients (P < 0.001). These results provide the first evidence that MTA3 expression was decreased in human glioma and negatively associated with prognosis of patients, suggesting that MTA3 may play a tumor suppressor role in glioma.
Abstract. Corosolic acid (CRA), a pentacyclic triterpene isolated from medicinal herbs, has been reported to exhibit anticancer properties in several cancers. However, the anticancer activity of CRA in osteosarcoma cells is still unclear. In the present study, the inhibitory effect of CRA in osteosarcoma MG-63 cells was investigated, and the results revealed that CRA significantly inhibited the viability of MG-63 cells in a dose-and time-dependent manner. A typical apoptotic hallmark such as DNA ladder was detected by agarose gel electrophoresis following treatment with CRA. Further experiments demonstrated that CRA induced apoptosis of MG-63 cells by flow cytometry using propidium iodide and annexin V staining. In addition, it was observed that the apoptosis of MG-63 cells induced by CRA was closely associated with activation of caspase-3 and caspase-9, loss of mitochondrial membrane potential, and release of cytochrome c from mitochondria, suggesting that CRA may trigger the activation of the mitochondria-mediated apoptosis pathway. In addition, the inhibition of caspase activity attenuated the CRA-induced apoptosis of MG-63 cells, which further confirmed the role of the mitochondrial pathway in CRA-induced apoptosis. These results indicated that CRA could induce the apoptosis of osteosarcoma cells through activating the mitochondrial pathway, which provides an evidence that CRA may be a useful chemotherapeutic agent for osteosarcoma.
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