Cell motility and cell stiffness are closely related to metastatic activity of cancer cells. (-)-Epigallocatechin gallate (EGCG) has been shown to inhibit spontaneous metastasis of melanoma cell line into the lungs of mice, so we studied the effects of EGCG on cell motility, cell stiffness, and expression of vimentin and Slug, which are molecular phenotypes of epithelial-mesenchymal transition (EMT). Treatments of human non-small cell lung cancer cell lines H1299 and Lu99 with 50 and 100 μM EGCG reduced cell motility to 67.5% and 43.7% in H1299, and 71.7% and 31.5% in Lu99, respectively in in vitro wound healing assay. Studies on cell stiffness using atomic force microscope (AFM) revealed that treatment with 50 μM EGCG increased Young's modulus of H1299 from 1.24 to 2.25 kPa and that of Lu99 from 1.29 to 2.28 kPa, showing a 2-fold increase in cell stiffness, i.e. rigid elasticity of cell membrane. Furthermore, treatment with 50 μM EGCG inhibited high expression of vimentin and Slug in the cells at a leading edge of scratch. Methyl-β-cyclodextrin, a reagent to deplete cholesterol in plasma membrane, showed inhibition of EMT phenotypes similar that by EGCG, suggesting that EGCG induces inhibition of EMT phenotypes by alteration of membrane organization.
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http://dx.doi.org/10.1016/j.bbrc.2013.10.094 | DOI Listing |
Materials (Basel)
January 2025
Department of Industrial Engineering, University of Trento, 38123 Trento, Italy.
The metastable β-Ti21S alloy exhibits a lower elastic modulus than Ti-6Al-4V ELI while maintaining high mechanical strength and ductility. To address stress shielding, this study explores the integration of lattice structures within prosthetics, which is made possible through additive manufacturing. Continuous adhesion between the implant and bone is essential; therefore, auxetic bow-tie structures with a negative Poisson's ratio are proposed for regions under tensile stress, while Triply Periodic Minimal Surface (TPMS) structures with a positive Poisson's ratio are recommended for areas under compressive stress.
View Article and Find Full Text PDFPolymers (Basel)
January 2025
Faculty of Physics, Lomonosov Moscow State University, Moscow 119991, Russia.
A finite element model of the local mechanical response of a filled polymer composite to uniaxial compression is presented. The interfacial layer between filler particles and polymer matrix is explicitly modeled as a third phase of the composite. Unit cells containing one or several anisometric filler particles surrounded by interface shells are considered.
View Article and Find Full Text PDFChembiochem
January 2025
Purdue University College of Engineering, Weldon School of Biomedical Engineering, 723 W. Michigan St., SL 220K, IN 46202, Indianapolis, UNITED STATES OF AMERICA.
Pancreatic ductal adenocarcinoma (PDAC) is marked by significant desmoplastic reactions, or the accumulation of excessive extracellular matrices. PDAC stroma has abnormally high stiffness, which alters cancer cell behaviors and creates a barrier for effective drug delivery. Unfortunately, clinical trials using a combination of chemotherapy and matrix-degrading enzyme have led to disappointing results, as the degradation of stromal tissue likely accelerated the dissemination of cancer cells.
View Article and Find Full Text PDFJ Biol Chem
January 2025
Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USA. Electronic address:
Extracellular matrix stiffness is one of the multiple mechanical signals that alters cellular behavior. During studies exploring the effect of matrix rigidity on lung fibroblast survival we discovered that enhanced survival on stiff substrates is dependent on elevated Ras activity, owing to the activation of the GEF, RasGRF1. Mechanistically, we found that the increased Ras activity lead to the activation of both the AKT and ERK pathways.
View Article and Find Full Text PDFJ Mol Cell Cardiol
January 2025
Shu Chien-Gene Lay Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093, USA; Institute of Engineering Medicine, University of California, San Diego, La Jolla, CA 92093, USA; Sanford Consortium for Regenerative Medicine, La Jolla, CA 92093, USA. Electronic address:
Vinculin (VCL) is a key adapter protein located in force-bearing costamere complexes, which mechanically couples the sarcomere to the ECM. Heterozygous vinculin frameshift genetic variants can contribute to cardiomyopathy when external stress is applied, but the mechanosensitive pathways underpinning VCL haploinsufficiency remain elusive. Here, we show that in response to extracellular matrix stiffening, heterozygous loss of VCL disrupts force-mediated costamere protein recruitment, thereby impairing cardiomyocyte contractility and sarcomere organization.
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