MTA1 promotes proliferation and invasion in human gastric cancer cells
Although metastasis-associated protein 1 (MTA1) has been widely linked to tumor metastasis, the relevant mechanisms remain to be elucidated, especially in gastric cancer. The aim of this study was to examine whether the MTA1 gene is associated with the process of proliferation and invasion by regula...
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Published in | OncoTargets and therapy Vol. 8; pp. 1785 - 1794 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
New Zealand
Dove Medical Press Limited
01.01.2015
Taylor & Francis Ltd Dove Medical Press |
Subjects | |
Online Access | Get full text |
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Summary: | Although metastasis-associated protein 1 (MTA1) has been widely linked to tumor metastasis, the relevant mechanisms remain to be elucidated, especially in gastric cancer. The aim of this study was to examine whether the MTA1 gene is associated with the process of proliferation and invasion by regulating several molecular targets in gastric cancer. MTA1 expression in 61 gastric cancer tissue and adjacent noncancerous tissues was analyzed by immunohistochemistry. The prognostic value of MTA1 for overall survival and disease-free survival was determined by Kaplan-Meier estimates, and the significance of differences between curves was evaluated by the log-rank test. Furthermore, overexpression of MTA1 in SGC7901 and BGC823 cells promoted cell cycle progression, cell adhesion, and cell invasion. Our study found that MTA1 is overexpressed in gastric cancers, which contributes to malignant cell growth by facilitating cell cycle progression through upregulation of cyclin D1 and accelerates the migration and invasion of human gastric cancer cells by regulating expression of fibronectin and MMP2/MMP9. Taken together, MTA1 was involved in the pathogenesis of gastric cancer and might be a candidate therapeutic target in gastric cancer. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Correction/Retraction-1 ObjectType-Feature-3 content type line 23 |
ISSN: | 1178-6930 1178-6930 |
DOI: | 10.2147/ott.s85383 |