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- Article] Myoferlin Depletion in Breast Cancer Cells Promotes Mesenchymal to Epithelial Shape Change and Stalls Invasion
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DocNo of ILP: 1266
Doc. Type: Article
Title: Myoferlin Depletion in Breast Cancer Cells Promotes Mesenchymal to Epithelial Shape Change and Stalls Invasion
Authors: Li, R; Ackerman, WE; Mihai, C; Volakis, LI; Ghadiali, S; Kniss, DA
Full Name of Authors: Li, Ruth; Ackerman, William E.; Mihai, Cosmin; Volakis, Leonithas I.; Ghadiali, Samir; Kniss, Douglas A.
Keywords by Author:
Keywords Plus: BASEMENT-MEMBRANE; MUSCULAR-DYSTROPHY; ENDOTHELIAL-CELLS; MUSCLE GROWTH; DYSFERLIN; REPAIR; METASTASIS; exPRESSION; FUSION; TUMOR
Abstract: Myoferlin (MYOF) is a mammalian ferlin protein with homology to ancestral Fer-1, a nematode protein that regulates spermatic membrane fusion, which underlies the amoeboid-like movements of its sperm. Studies in muscle and endothelial cells have reported on the role of myoferlin in membrane repair, endocytosis, myoblast fusion, and the proper expression of various plasma membrane receptors. In this study, using an in vitro human breast cancer cell model, we demonstrate that myoferlin is abundantly expressed in invasive breast tumor cells. Depletion of MYOF using lentiviral-driven shRNA expression revealed that MDA-MB-231 cells reverted to an epithelial morphology, suggesting at least some features of mesenchymal to epithelial transition (MET). These observations were confirmed by the down-regulation of some mesenchymal cell markers (e.g., fibronectin and vimentin) and coordinate up-regulation of the E-cadherin epithelial marker. Cell invasion assays using Boyden chambers showed that loss of MYOF led to a significant diminution in invasion through Matrigel or type I collagen, while cell migration was unaffected. PCR array and screening of serum-free culture supernatants from shRNA(MYOF) transduced MDA-MB-231 cells indicated a significant reduction in the steady-state levels of several matrix metalloproteinases. These data when considered in toto suggest a novel role of MYOF in breast tumor cell invasion and a potential reversion to an epithelial phenotype upon loss of MYOF.
Cate of OECD: Other natural sciences
Year of Publication: 2012
Business Area: other
Detail Business: medicine & science
Country: USA
Study Area:
Name of Journal: PLOS ONE
Language: English
Country of Authors: [Li, Ruth; Ackerman, William E.; Kniss, Douglas A.] Ohio State Univ, Dept Obstet & Gynecol, Div Maternal Fetal Med, Lab Perinatal Res, Columbus, OH 43210 USA; [Volakis, Leonithas I.; Ghadiali, Samir; Kniss, Douglas A.] Ohio State Univ, Dept Biomed Engn, Columbus, OH 43210 USA; [Ghadiali, Samir] Ohio State Univ, Dept Internal Med, Div Pulm Allergy Crit Care & Sleep Med, Columbus, OH 43210 USA; [Mihai, Cosmin] Pacific NW Natl Lab, Richland, WA 99352 USA
Press Adress: Li, R (reprint author), Ohio State Univ, Dept Obstet & Gynecol, Div Maternal Fetal Med, Lab Perinatal Res, Columbus, OH 43210 USA.
Email Address: kniss.1@osu.edu
Citaion:
Funding: Ohio State University; NIH [K08 HD49628]; National Science Foundation Nanoscience Science and Engineering Center [EEC-0425626]; Chemical, Bioengineering, Environmental, and Transport Systems (CBET) [1134201]
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Number of Citaion: 54
Publication: PUBLIC LIBRARY SCIENCE
City of Publication: SAN FRANCISCO
Address of Publication: 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
ISSN: 1932-6203
29-Character Source Abbreviation: PLOS ONE
ISO Source Abbreviation: PLoS One
Volume: 7
Version: 6
Start of File:
End of File:
DOI: 10.1371/journal.pone.0039766
Number of Pages: 12
Web of Science Category: Multidisciplinary Sciences
Subject Category: Science & Technology - Other Topics
Document Delivery Number: 966GL
Unique Article Identifier: WOS:000305825800067
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