ArticleCellular and molecular bioengineering2020
Differential Contributions of Actin and Myosin to the Physical Phenotypes and Invasion of Pancreatic Cancer Cells.
Article in Cellular and molecular bioengineering, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Review
- Deformability screening identifies NUDT5 as a mediator of cellular mechanobiology.bioRxiv : the preprint server for biology · 2026Article
- β-adrenergic signaling modulates breast cancer cell mechanical behaviors through a RhoA-ROCK-myosin II axis.iScience · 2025Article
- Altered Mechanobiology of PDAC Cells with Acquired Chemoresistance to Gemcitabine and Paclitaxel.Cancers · 2024Article
- The Inhibition of Vessel Co-Option as an Emerging Strategy for Cancer Therapy.International journal of molecular sciences · 2024Review
- Molecular determinants of intrinsic cellular stiffness in health and disease.Biophysical reviews · 2022Review
- Review
- Mechanical Stress Signaling in Pancreatic Cancer Cells Triggers p38 MAPK- and JNK-Dependent Cytoskeleton Remodeling and Promotes Cell Migration via Rac1/cdc42/Myosin II.Molecular cancer research : MCR · 2022Article
- Pancreatic Ductal Adenocarcinoma Cortical Mechanics and Clinical Implications.Frontiers in oncology · 2022Review
- Cancer-Nano-Interaction: From Cellular Uptake to Mechanobiological Responses.International journal of molecular sciences · 2021Review
- A constriction channel analysis of astrocytoma stiffness and disease progression.Biomicrofluidics · 2021Article
- Effects of energy metabolism on the mechanical properties of breast cancer cells.Communications biology · 2020Article
- Cancer cells optimize elasticity for efficient migration.Royal Society open science · 2020Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
introductionMetastasis is a fundamentally physical process in which cells deform through narrow gaps and generate forces to invade surrounding tissues. While it is commonly thought that increased cell deformability is an advantage for invading cells, we previously found that more invasive pancreatic ductal adenocarcinoma (PDAC) cells are stiffer than less invasive PDAC cells. Here we investigate potential mechanisms of the simultaneous increase in PDAC cell stiffness and invasion, focusing on the contributions of myosin II, Arp2/3, and formins.
methodWe measure cell invasion using a 3D scratch wound invasion assay and cell stiffness using atomic force microscopy (AFM). To determine the effects of actin- and myosin-mediated force generation on cell stiffness and invasion, we treat cells with pharmacologic inhibitors of myosin II (blebbistatin), Arp2/3 (CK-666), and formins (SMIFH2).
resultsWe find that the activity of myosin II, Arp2/3, and formins all contribute to the stiffness of PDAC cells. Interestingly, we find that the invasion of PDAC cell lines is differentially affected when the activity of myosin II, Arp2/3, or formins is inhibited, suggesting that despite having similar tissue origins, different PDAC cell lines may rely on different mechanisms for invasion.
conclusionsThese findings deepen our knowledge of the factors that regulate cancer cell mechanotype and invasion, and incite further studies to develop therapeutics that target multiple mechanisms of invasion for improved clinical benefit.
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