Substrate flexibility regulates growth and apoptosis of normal but not transformed cells.

By Hong-Bei Wang, Micah Dembo, Yu-li Wang. American Journal of Physiology - Cell Physiology, 2000

652 citations recorded by the source corpus.

Subfields: Biomaterials, Cell Biology, Immunology and Allergy

View Paper: https://www.semanticscholar.org/paper/a1be1e36e900c83ee596a12208ab4c74a3e7f01c

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Citations in the corpus

Tensional homeostasis and the malignant phenotype. (2005, background): “…and CANCER CELL : SEPTEMBER 2005 249 survive in the absence of exogenous matrix tension (i.e., in suspension ), fail to undergo differentiation in compliant 3D ECMs, and have elevated FAK pY397 in culture and in vivo (Lark et al., 2005; McLean et al., 2004; Wang et al., 2000; Wozniak et al., 2003).”
Harnessing nanotopography and integrin-matrix interactions to influence stem cell fate. (2014, background): “smooth muscle cells [31, 53], and transformed cells [67, 125].”
The mechanical rigidity of the extracellular matrix regulates the structure, motility, and proliferation of glioma cells (2009, background): “of this effect is somewhat surprising, ECM rigidity has been observed to modulate cell growth in other systems, including fibroblasts (44), hepatocytes (45), and neural stem cells (46).”
Effects of substrate stiffness on cell morphology, cytoskeletal structure, and adhesion. (2005, methodology): “…matrix, in contrast to the growth of cultured cells at a solid/liquid interface [Bard and Hay, 1975; Greenburg and Hay, 1982], but an additional independent difference relates to differences in elasticity of biological surfaces [Lo et al., 2000; Pelham and Wang 1997; Wang et al., 2000a].”
Feedback amplification of fibrosis through matrix stiffening and COX-2 suppression (2010, background): “Although prior work has established that fibroblast proliferation and myofibroblast differentiation vary with matrix stiffness (Arora et al., 1999; Wang et al., 2000; Goffin et al., 2006; Li et al., 2007), our work shows for the first time that fibro-”
Mechanics, malignancy, and metastasis: The force journey of a tumor cell (2009, background): “When presented with compliant substrates that suppress spreading and proliferation of normal cells, transformed cells both proliferate extensively [22] and exert abnormally high tractional forces, which can in turn disrupt cell-cell junctional integrity, compromise tissue polarity, promote anchorage”
Review on Cell Mechanics: Experimental and Modeling Approaches (2013, methodology): “…been used to measure the forces produced by a vast number of different cell types [254,367,376–379], to determine the contribution of active cytoskeletal contraction to these traction forces [377] [380] [381], and to elucidate the effects of pathological events on these forces [382] [383] [384].”
Schwarz meets Schwann: Design and fabrication of biomorphic and durataxic tissue engineering scaffolds (2006, background): “, 2000; Georges and Janmey, 2005), apoptosis (Wang et al., 2000), phagocytosis (Beningo and Wang, 2002) and normal differentiation (Cukiermen et al.”
Nascent Focal Adhesions Are Responsible for the Generation of Strong Propulsive Forces in Migrating Fibroblasts (2001, methodology): “This flexibility was high enough to allow reliable determination of traction-induced deformation, but not to induce drastic changes in cell morphology or growth as reported previously with softer surfaces (Pelham and Wang, 1997; Wang et al., 2000).”