ArticleNature materials2022
Correlative cryo-ET identifies actin/tropomyosin filaments that mediate cell-substrate adhesion in cancer cells and mechanosensitivity of cell proliferation.
Article in Nature materials, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Transient Cytoskeletal Anisotropy Encodes Short-Term Mechanical Memory in Glioblastoma Cells.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Revealing biomechanical vulnerabilities in oral cancer cells using 3D coculture platform and low-frequency ultrasound.Materials today. Bio · 2026Article
- Single Cell Mechanics in Disease Progression.Small science · 2026Review
- The Sole Essential Low Molecular Weight Tropomyosin Isoform of Caenorhabditis elegans Is Essential for Pharyngeal Muscle Function.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Heterogeneous focal adhesion cytoskeleton nanoarchitectures from microengineered interfacial curvature to oversee nuclear remodeling and mechanotransduction of mesenchymal stem cells.Cellular & molecular biology letters · 2025Article
- Human congenital cataract mutation inInternational journal of ophthalmology · 2025Article
- Single molecule visualization of tropomyosin isoform organization in the mammalian actin cytoskeleton.Cytoskeleton (Hoboken, N.J.) · 2025Article
- The sole essential low molecular weight tropomyosin isoform ofbioRxiv : the preprint server for biology · 2024Article
- Functional and Structural Properties of Cytoplasmic Tropomyosin Isoforms Tpm1.8 and Tpm1.9.International journal of molecular sciences · 2024Article
- Functional meniscus reconstruction with biological and biomechanical heterogeneities through topological self-induction of stem cells.Bioactive materials · 2024Article
- Young osteocyte-derived extracellular vesicles facilitate osteogenesis by transferring tropomyosin-1.Journal of nanobiotechnology · 2024Article
- Mechanical stability of polarization signatures in biological tissue characterization.Biomedical optics express · 2024Article
- Focal adhesions contain three specialized actin nanoscale layers.Nature communications · 2024Article
- Tropomyosin1 isoforms underlie epithelial to mesenchymal plasticity, metastatic dissemination, and resistance to chemotherapy in high-grade serous ovarian cancer.Cell death and differentiation · 2024Article
- Article
- Impairment of rigidity sensing caused by mutant TP53 gain of function in osteosarcoma.Bone research · 2023Article
- Identification of a novel circRNA-miRNA-mRNA regulatory axis in hepatocellular carcinoma based on bioinformatics analysis.Scientific reports · 2023Article
- TPM2 attenuates progression of prostate cancer by blocking PDLIM7-mediated nuclear translocation of YAP1.Cell & bioscience · 2023Article
- AZGP1P2/UBA1/RBM15 Cascade Mediates the Fate Determinations of Prostate Cancer Stem Cells and Promotes Therapeutic Effect of Docetaxel in Castration-Resistant Prostate Cancer via TPM1 m6A Modification.Research (Washington, D.C.) · 2023Article
- Caldesmon controls stress fiber force-balance through dynamic cross-linking of myosin II and actin-tropomyosin filaments.Nature communications · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The actin cytoskeleton is the primary driver of cellular adhesion and mechanosensing due to its ability to generate force and sense the stiffness of the environment. At the cell's leading edge, severing of the protruding Arp2/3 actin network generates a specific actin/tropomyosin (Tpm) filament population that controls lamellipodial persistence. The interaction between these filaments and adhesion to the environment is unknown. Using cellular cryo-electron tomography we resolve the ultrastructure of the Tpm/actin copolymers and show that they specifically anchor to nascent adhesions and are essential for focal adhesion assembly. Re-expression of Tpm1.8/1.9 in transformed and cancer cells is sufficient to restore cell-substrate adhesions. We demonstrate that knock-out of Tpm1.8/1.9 disrupts the formation of dorsal actin bundles, hindering the recruitment of α-actinin and non-muscle myosin IIa, critical mechanosensors. This loss causes a force-generation and proliferation defect that is notably reversed when cells are grown on soft surfaces. We conclude that Tpm1.8/1.9 suppress the metastatic phenotype, which may explain why transformed cells naturally downregulate this Tpm subset during malignant transformation.
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