Expression of metastasis-associated protein 3 in human brain glioma related to tumor prognosis.

Neurol Sci

Qingdao First Sanatorium of Jinan Military Region, Qingdao, 266071, Shandong, People's Republic of China.

Published: October 2015

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.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s10072-015-2252-8DOI Listing

Publication Analysis

Top Keywords

mta3 expression
16
metastasis-associated protein
8
clinical significance
8
human malignancies
8
mta3
8
mta3 play
8
human glioma
8
expression decreased
8
expression
7
glioma
7

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!