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novel function of sJAM-C in promoting cytoskeleton rearrangement and migration in mammary epithelial cells
- 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 |
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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. |
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Subject(s): |
Tight junctions (Cell biology) Cell interaction Cell junction Cell adhesion Microcirculation |
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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 |