Periostin-binding DNA Aptamer Inhibits Breast Cancer Growth and Metastasis
Cited 7 times inCited 7 times in
- Periostin-binding DNA Aptamer Inhibits Breast Cancer Growth and Metastasis
- Lee, Yu Jin; Kim, Il Shin; Park, Soo-Ah; Kim, Youndong; Lee, Jeung Eun; Noh, Dong-Young; Kim, Kyong-Tai; Ryu, Sung Ho; Suh, Pann-Ghill
- Issue Date
- NATURE PUBLISHING GROUP
- MOLECULAR THERAPY, v.21, no.5, pp.1004 - 1013
- Periostin is an extracellular matrix (ECM) protein that is overexpressed in a variety of human cancers, and its functions appear to be linked to tumor growth, metastasis, and angiogenesis. Recent clinical evidence suggests that aberrant periostin expression is correlated with poor outcome in patients with breast cancer. To identify novel tools to regulate the functional role of periostin, we generated benzyl-d(U)TP-modified DNA aptamers that were directed against human periostin (PNDAs) and characterized their functional roles in breast cancer progression. PNDA-3 selectively bound to the FAS-1 domain of periostin with nanomolar affinity and disrupted the interaction between periostin and its cell surface receptors, alpha(v)beta(3) and alpha(v)beta(5) integrins. PNDA-3 markedly antagonized the periostin-induced adhesion, migration, and invasion of breast cancer cells and blocked the activation of various components of the alpha(v)beta(3) and alpha(v)beta(5) integrin signal transduction pathways. In a 4T1 orthotopic mouse model, PNDA-3 administration significantly reduced primary tumor growth and distant metastasis. Thus, our results demonstrated that periostin-integrin signaling regulates breast cancer progression at multiple levels in tumor cells and the tumor microenvironment. DNA aptamers targeting periostin may potentially be used to inhibit breast cancer progression.
- Appears in Collections:
- BIO_Journal Papers
- Files in This Item:
- There are no files associated with this item.
can give you direct access to the published full text of this article. (UNISTARs only)
Show full item record
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.