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- W2071853778 abstract "During tumorigenesis, matrix rigidity can drive oncogenic transformation via altered cellular proliferation and migration. Cells sense extracellular matrix (ECM) mechanical properties with intracellular tensile forces generated by actomyosin contractility. These contractile forces are transmitted to the matrix surface as traction stresses, which mediate mechanical interactions with the ECM. Matrix rigidity has been shown to increase proteolytic ECM degradation by cytoskeletal structures known as invadopodia that are critical for cancer progression, suggesting that cellular contractility promotes invasive behavior. However, both increases and decreases in traction stresses have been associated with metastatic behavior. Therefore, the role of cellular contractility in invasive migration leading to metastasis is unclear. To determine the relationship between cellular traction stresses and invadopodia activity, we characterized the invasive and contractile properties of an aggressive carcinoma cell line utilizing polyacrylamide gels of different rigidities. We found that ECM degradation and traction stresses were linear functions of matrix rigidity. Using calyculin A to augment myosin contractility, we also found that traction stresses were strongly predictive of ECM degradation. Overall, our data suggest that cellular force generation may play an important part in invasion and metastasis by mediating invadopodia activity in response to the mechanical properties of the tumor microenvironment." @default.
- W2071853778 created "2016-06-24" @default.
- W2071853778 creator A5048607111 @default.
- W2071853778 creator A5056472764 @default.
- W2071853778 date "2014-05-01" @default.
- W2071853778 modified "2023-10-16" @default.
- W2071853778 title "Cellular traction stresses mediate extracellular matrix degradation by invadopodia" @default.
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- W2071853778 doi "https://doi.org/10.1016/j.actbio.2013.12.058" @default.
- W2071853778 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3976707" @default.
- W2071853778 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24412623" @default.
- W2071853778 hasPublicationYear "2014" @default.
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