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novel function of sJAM-C in promoting cytoskeleton rearrangement and migration in mammary epithelial cells

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Date Issued:
2012
Summary:
Soluble form of Junctional adhesion molecule C (sJAM-C) has been identified to cause angiogenesis as well as chemotaxis in endothelial cells. However, the role of sJAM-C in the context of cancer has not been elucidated. Our atomic force microscopy (AFM) stiffness measurements of normal mammary epithelial cells (MCF 10A) have shown a two-fold decrease in cell's stiffness in response to sJAM-C. Changes in cell stiffness are indicative of modulations in a cell's mechanical properties. Our results indicated that sJAM-C increased the MCF 10A cell migration about two-fold and also promoted a three-fold increase in chemotaxis. Additionally, sJAM-C treatment resulted in considerable filamentous-actin loss and peripheral actin ring breakage. We also found activation of Rho signaling pathway to be the main mechanism behind sJAM-C mediated alterations in MCF 10A cell cytoskeleton and motility. Our data present for the first time that sJAM-C is a pro metastatic mediator for normal mammary epithelial cells.
Title: The novel function of sJAM-C in promoting cytoskeleton rearrangement and migration in mammary epithelial cells.
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Name(s): Qureshi, Anila
Charles E. Schmidt College of Medicine
Department of Biomedical Science
Type of Resource: text
Genre: Electronic Thesis Or Dissertation
Date Issued: 2012
Publisher: Florida Atlantic University
Physical Form: electronic
Extent: vii, 40 p. : ill. (some col.)
Language(s): English
Summary: Soluble form of Junctional adhesion molecule C (sJAM-C) has been identified to cause angiogenesis as well as chemotaxis in endothelial cells. However, the role of sJAM-C in the context of cancer has not been elucidated. Our atomic force microscopy (AFM) stiffness measurements of normal mammary epithelial cells (MCF 10A) have shown a two-fold decrease in cell's stiffness in response to sJAM-C. Changes in cell stiffness are indicative of modulations in a cell's mechanical properties. Our results indicated that sJAM-C increased the MCF 10A cell migration about two-fold and also promoted a three-fold increase in chemotaxis. Additionally, sJAM-C treatment resulted in considerable filamentous-actin loss and peripheral actin ring breakage. We also found activation of Rho signaling pathway to be the main mechanism behind sJAM-C mediated alterations in MCF 10A cell cytoskeleton and motility. Our data present for the first time that sJAM-C is a pro metastatic mediator for normal mammary epithelial cells.
Identifier: 856903285 (oclc), 3362046 (digitool), FADT3362046 (IID), fau:4160 (fedora)
Note(s): by Anila Qureshi.
Thesis (M.S.)--Florida Atlantic University, 2012.
Includes bibliography.
Mode of access: World Wide Web.
System requirements: Adobe Reader.
Subject(s): Tight junctions (Cell biology)
Cell interaction
Cell junction
Cell adhesion
Microcirculation
Persistent Link to This Record: http://purl.flvc.org/fcla/dt/3362046
Use and Reproduction: http://rightsstatements.org/vocab/InC/1.0/
Host Institution: FAU