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      High-frequency microrheology in 3D reveals mismatch between cytoskeletal and extracellular matrix mechanics

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      Proceedings of the National Academy of Sciences
      Proceedings of the National Academy of Sciences

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          Abstract

          Mechanical homeostasis describes how cells sense physical cues from the microenvironment and concomitantly remodel both the cytoskeleton and the surrounding extracellular matrix (ECM). Such feedback is thought to be essential to healthy development and maintenance of tissue. However, the nature of the dynamic coupling between microscale cell and ECM mechanics remains poorly understood. Here we investigate how and whether cells remodel their cortex and basement membrane to adapt to their microenvironment. We measured both intracellular and extracellular viscoelasticity, generating a full factorial dataset on 5 cell lines in 2 ECMs subjected to 4 cytoskeletal drug treatments at 2 time points. Nonmalignant breast epithelial cells show a similar viscoelasticity to that measured for the local ECM when cultured in 3D laminin-rich ECM. In contrast, the malignant counterpart is stiffer than the local environment. We confirmed that other mammary cancer cells embedded in tissue-mimetic hydrogels are nearly 4-fold stiffer than the surrounding ECM. Perturbation of actomyosin did not yield uniform responses but instead depended on the cell type and chemistry of the hydrogel. The observed viscoelasticity of both ECM and cells were well described by power laws in a frequency range that governs single filament cytoskeletal dynamics. Remarkably, the intracellular and extracellular power law parameters for the entire dataset collectively fall onto 2 parallel master curves described by just 2 parameters. Our work shows that tumor cells are mechanically plastic to adapt to many environments and reveals dynamical scaling behavior in the microscale mechanical responses of both cells and ECM.

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          Most cited references21

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          Tensional homeostasis and the malignant phenotype.

          Tumors are stiffer than normal tissue, and tumors have altered integrins. Because integrins are mechanotransducers that regulate cell fate, we asked whether tissue stiffness could promote malignant behavior by modulating integrins. We found that tumors are rigid because they have a stiff stroma and elevated Rho-dependent cytoskeletal tension that drives focal adhesions, disrupts adherens junctions, perturbs tissue polarity, enhances growth, and hinders lumen formation. Matrix stiffness perturbs epithelial morphogenesis by clustering integrins to enhance ERK activation and increase ROCK-generated contractility and focal adhesions. Contractile, EGF-transformed epithelia with elevated ERK and Rho activity could be phenotypically reverted to tissues lacking focal adhesions if Rho-generated contractility or ERK activity was decreased. Thus, ERK and Rho constitute part of an integrated mechanoregulatory circuit linking matrix stiffness to cytoskeletal tension through integrins to regulate tissue phenotype.
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            Human breast cancer invasion and aggression correlates with ECM stiffening and immune cell infiltration.

            Tumors are stiff and data suggest that the extracellular matrix stiffening that correlates with experimental mammary malignancy drives tumor invasion and metastasis. Nevertheless, the relationship between tissue and extracellular matrix stiffness and human breast cancer progression and aggression remains unclear. We undertook a biophysical and biochemical assessment of stromal-epithelial interactions in noninvasive, invasive and normal adjacent human breast tissue and in breast cancers of increasingly aggressive subtype. Our analysis revealed that human breast cancer transformation is accompanied by an incremental increase in collagen deposition and a progressive linearization and thickening of interstitial collagen. The linearization of collagen was visualized as an overall increase in tissue birefringence and was most striking at the invasive front of the tumor where the stiffness of the stroma and cellular mechanosignaling were the highest. Amongst breast cancer subtypes we found that the stroma at the invasive region of the more aggressive Basal-like and Her2 tumor subtypes was the most heterogeneous and the stiffest when compared to the less aggressive luminal A and B subtypes. Intriguingly, we quantified the greatest number of infiltrating macrophages and the highest level of TGF beta signaling within the cells at the invasive front. We also established that stroma stiffness and the level of cellular TGF beta signaling positively correlated with each other and with the number of infiltrating tumor-activated macrophages, which was highest in the more aggressive tumor subtypes. These findings indicate that human breast cancer progression and aggression, collagen linearization and stromal stiffening are linked and implicate tissue inflammation and TGF beta.
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              Scaling the microrheology of living cells.

              We report a scaling law that governs both the elastic and frictional properties of a wide variety of living cell types, over a wide range of time scales and under a variety of biological interventions. This scaling identifies these cells as soft glassy materials existing close to a glass transition, and implies that cytoskeletal proteins may regulate cell mechanical properties mainly by modulating the effective noise temperature of the matrix. The practical implications are that the effective noise temperature is an easily quantified measure of the ability of the cytoskeleton to deform, flow, and reorganize.
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                Author and article information

                Journal
                Proceedings of the National Academy of Sciences
                Proc Natl Acad Sci USA
                Proceedings of the National Academy of Sciences
                0027-8424
                1091-6490
                July 16 2019
                July 16 2019
                July 16 2019
                July 02 2019
                : 116
                : 29
                : 14448-14455
                Article
                10.1073/pnas.1814271116
                6642418
                31266897
                89594b03-5aca-4cc9-a0b4-b4edac8992ad
                © 2019

                Free to read

                https://www.pnas.org/site/aboutpnas/licenses.xhtml

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