ArticleBMC biology2025
High matrix stiffness accelerates migration of hepatocellular carcinoma cells through the integrin β1-Plectin-F-actin axis.
Article in BMC biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Matrix stiffness-induced YEATS2 drives HCC progression via epigenetic activation of the TGFBR2-TAZ-AKT pathway.Cell death and differentiation · 2026Article
- Plectin-mediated mitochondrial fusion is necessary for hepatocellular carcinoma cell migration promoted by higher matrix stiffness.Histochemistry and cell biology · 2026Article
- Disulfidptosis-related gene DSTN predicts prognosis and promotes malignant progression in head and neck squamous cell carcinoma.Molecular and cellular biochemistry · 2026Article
- Article
- The movement imperative: reimagining healthcare through the lens of human movement.Frontiers in sports and active living · 2026Review
- The role of plectin as a druggable target in papillary thyroid carcinoma: therapeutic potential of troglitazone.Frontiers in immunology · 2026Article
- Microenvironmental and Molecular Pathways Driving Dormancy Escape in Bone Metastases.International journal of molecular sciences · 2025Review
- The plakin family: Potential therapeutic targets for digestive system tumors.Journal of translational internal medicine · 2025Article
- The Role of Plectin Dysregulation in Cancer: Recent Advances.Molecules (Basel, Switzerland) · 2025Review
- Biomechanics of the tumor extracellular matrix and regulatory T cells: regulatory mechanisms and potential therapeutic targets.Cell communication and signaling : CCS · 2025Review
- Extracellular matrix stiffness regulates the proliferation and migration capacities of lymphatic endothelial cells via FAT1.Frontiers in cell and developmental biology · 2025Article
- ECM remodeling in hypothyroidism-associated MAFLD: mechanisms, clinical relevance, and therapeutic targets.Frontiers in immunology · 2025Review
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Authors and funding
4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundAbundant research indicates that increased extracellular matrix (ECM) stiffness significantly enhances the malignant characteristics of hepatocellular carcinoma (HCC) cells. Plectin, an essential cytoskeletal linker protein, has recently emerged as a promoter of cancer progression, particularly in the context of cancer cell invasion and metastasis. However, the responsiveness of plectin to changes in ECM stiffness and its impact on HCC progression remain unclear. In this study, we aimed to investigate whether plectin responds to variations in ECM stiffness and to explore its involved molecular mechanisms in regulating HCC cell migration.
resultsOur results showed that, when compared with control group (7 kPa), high ECM stiffness (53 kPa) boosts HCC cell migration by upregulating plectin and integrin β1 expression and increasing F-actin polymerization. Knockdown of integrin β1 negated the high stiffness-upregulated plectin expression. Furthermore, reducing either plectin or integrin β1 levels, or using latrunculin A, effectively prevented the high ECM stiffness-induced F-actin polymerization and HCC cell migration.
conclusionsThese findings demonstrate that integrin β1-plectin-F-actin axis is necessary for high matrix stiffness-driven migration of HCC cells, and provide evidence for the critical role of plectin in mechanotransduction in HCC cells.
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