Journal
PLOS ONE
Volume 13, Issue 3, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0194170
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Funding
- National Science Foundation MultiSTEPS IGERT DGE Grant [0966125]
- Center for Engineered Health (Virginia Tech Institute for Critical Technology and Applied Science) (ICTAS)
- USDA National Institute of Food and Agriculture Hatch project [1006578]
- Fralin Life Science Institute
- Virginia Polytechnic Institute
- State University
- Direct For Education and Human Resources
- Division Of Graduate Education [0966125] Funding Source: National Science Foundation
- Div Of Molecular and Cellular Bioscience
- Direct For Biological Sciences [1517506] Funding Source: National Science Foundation
- NIFA [1006578, 812709] Funding Source: Federal RePORTER
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Ovarian cancer cells are exposed to physical stress in the peritoneal cavity during both tumor growth and dissemination. Ascites build-up in metastatic ovarian cancer further increases the exposure to fluid shear stress. Here, we used a murine, in vitro ovarian cancer progression model in parallel with immortalized human cells to investigate how ovarian cancer cells of increasing aggressiveness respond to < 1 dyne/cm(2)of fluid-induced shear stress. This biophysical stimulus significantly reduced cell viability in all cells exposed, independent of disease stage. Fluid shear stress induced spheroid formation and altered cytoskeleton organization in more tumorigenic cell lines. While benign ovarian cells appeared to survive in higher numbers under the influence of fluid shear stress, they exhibited severe morphological changes and chromosomal instability. These results suggest that exposure of benign cells to low magnitude fluid shear stress can induce phenotypic changes that are associated with transformation and ovarian cancer progression. Moreover, exposure of tumorigenic cells to fluid shear stress enhanced anchorage-independent survival, suggesting a role in promoting invasion and metastasis.
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