Oxytocin (OT) inhibits the proliferation of breast-cancer cells in vitro via a specific G-coupled receptor. To elucidate the intracellular mechanism involved in this biological effect, different G-coupled receptor mediators have been investigated in untreated and OT-treated MDA-MB231 breastcarcinoma
Novobiocin decreases SMYD3 expression and inhibits the migration of MDA-MB-231 human breast cancer cells
✍ Scribed by Xue-Gang Luo; Jia-Ning Zou; Shu-Zhen Wang; Tong-Cun Zhang; Tao Xi
- Publisher
- John Wiley and Sons
- Year
- 2009
- Tongue
- English
- Weight
- 275 KB
- Volume
- 62
- Category
- Article
- ISSN
- 1521-6543
- DOI
- 10.1002/iub.288
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
SET and MYND domain‐containing protein 3 (SMYD3) is a histone methyltransferase that plays an important role in transcriptional regulation in human carcinogenesis, and heat‐shock protein HSP90A has been shown to increase the activity of SMYD3. We previously reported that overexpression of SMYD3 stimulated the migration of cells. In this study, we further found that novobiocin, a HSP90 inhibitor, could decrease the expression of SMYD3 and dose dependently inhibit the proliferation and migration of MDA‐MB‐231 human breast cancer cells. As a control, the short hairpin RNA (shRNA) targeting SMYD3 gene also showed similar effects with novobicin. This study is the first to show that novobiocin can inhibit the migration of breast cancer cells and such event may involve the downregulation of SMYD3. These findings might throw light on the development of novel therapeutic approaches to human cancers, and lend further understanding to the potential role of SMYD3 in human carcinogenesis. © 2009 IUBMB IUBMB Life, 62(3): 194–199, 2010
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