Matrix metalloproteinase-2 regulates MDA-MB-231 breast cancer cell invasion induced by active mammalian diaphanous-related formin 1open access
- Authors
- Kim, Daehwan; Rhee, Sangmyung
- Issue Date
- Jul-2016
- Publisher
- SPANDIDOS PUBL LTD
- Keywords
- formin; mammalian diaphanous-related formin 1; breast cancer cells; matrix metalloproteinase-2; invasion
- Citation
- MOLECULAR MEDICINE REPORTS, v.14, no.1, pp 277 - 282
- Pages
- 6
- Journal Title
- MOLECULAR MEDICINE REPORTS
- Volume
- 14
- Number
- 1
- Start Page
- 277
- End Page
- 282
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/6774
- DOI
- 10.3892/mmr.2016.5282
- ISSN
- 1791-2997
1791-3004
- Abstract
- Mammalian diaphanous-related formin 1 (mDia1) was initially identified as a Rho GTPase effector involved in the progression of various diseases, including types of cancer. However, the precise underlying molecular mechanism of mDia1-mediated cancer cell invasion remains to be elucidated. In the present study, mDia1 expression was demonstrated to be upregulated in tissues from a number of cancer types, including kidney, prostate, and breast cancer using immunohistochemical analysis. Forced expression of a constitutively active (CA) form of mDia1 induces invasion, as measured by Transwell invasion assay, of MDA-MB-231 cells, which is a highly invasive breast cancer cell line, and this effect was markedly impaired by matrix metalloproteinase (MMP)-2 silencing. Furthermore, the present study demonstrated that overexpression of the CA form of mDia1 leads to the induction of invasive ability in MCF-7 cells, which is a non-invasive breast cancer cell line, as a result of increased MMP-2 activity. Thus, the results of the current study suggest that mDia1 is an important regulator of breast cancer cell invasion and that this effect may be mediated by MMP-2 activity.
- Files in This Item
-
- Appears in
Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.