ArticlePloS one2012
Matrix-bound PAI-1 supports cell blebbing via RhoA/ROCK1 signaling.
Article in PloS one, 2012. 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, 34 citations in OpenAlex.
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- Whole blood gene expression analysis of spontaneous hypertriglyceridemia in dogs suggests an underlying pro-thrombotic process.PloS one · 2024Article
- Platelet Microvesicles, Inflammation, and Coagulation Markers: A Pilot Study.Hematology reports · 2023Article
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- Plasticity of cancer cell invasion: Patterns and mechanisms.Translational oncology · 2021Review
- WNT11-FZD7-DAAM1 signalling supports tumour initiating abilities and melanoma amoeboid invasion.Nature communications · 2020Article
- Molecular biomarkers of Graves' ophthalmopathy.Experimental and molecular pathology · 2019Review
- KIF13A-regulated RhoB plasma membrane localization governs membrane blebbing and blebby amoeboid cell migration.The EMBO journal · 2018Article
- TGF-β1/p53 signaling in renal fibrogenesis.Cellular signalling · 2018Review
- The crosstalk between breast carcinoma-associated fibroblasts and cancer cells promotes RhoA-dependent invasionOncotarget · 2018Article
- Integration of Canonical and Noncanonical Pathways in TLR4 Signaling: Complex Regulation of the Wound Repair Program.Advances in wound care · 2017Review
- ROCK-1 mediates diabetes-induced retinal pigment epithelial and endothelial cell blebbing: Contribution to diabetic retinopathy.Scientific reports · 2017Article
- GnRH Induces ERK-Dependent Bleb Formation in Gonadotrope Cells, Involving Recruitment of Members of a GnRH Receptor-Associated Signalosome to the Blebs.Frontiers in endocrinology · 2017Article
- High glucose and insulin enhance uPA expression, ROS formation and invasiveness in breast cancer-derived cells.Cellular oncology (Dordrecht, Netherlands) · 2016Article
- Insulin augments serotonin-induced contraction via activation of the IR/PI3K/PDK1 pathway in the rat carotid artery.Pflugers Archiv : European journal of physiology · 2016Article
- The basic helix-loop-helix/leucine zipper transcription factor USF2 integrates serum-induced PAI-1 expression and keratinocyte growth.Journal of cellular biochemistry · 2014Article
- Silencing of TBC1D15 promotes RhoA activation and membrane blebbing.Molecular and cellular biochemistry · 2014Article
- The receptor for urokinase-plasminogen activator (uPAR) controls plasticity of cancer cell movement in mesenchymal and amoeboid migration style.Oncotarget · 2014Article
- SERPINE1: A Molecular Switch in the Proliferation-Migration Dichotomy in Wound-"Activated" Keratinocytes.Advances in wound care · 2014Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
The microenvironment of a tumor can influence both the morphology and the behavior of cancer cells which, in turn, can rapidly adapt to environmental changes. Increasing evidence points to the involvement of amoeboid cell migration and thus of cell blebbing in the metastatic process; however, the cues that promote amoeboid cell behavior in physiological and pathological conditions have not yet been clearly identified. Plasminogen Activator Inhibitor type-1 (PAI-1) is found in high amount in the microenvironment of aggressive tumors and is considered as an independent marker of bad prognosis. Here we show by immunoblotting, activity assay and immunofluorescence that, in SW620 human colorectal cancer cells, matrix-associated PAI-1 plays a role in the cell behavior needed for amoeboid migration by maintaining cell blebbing, localizing PDK1 and ROCK1 at the cell membrane and maintaining the RhoA/ROCK1/MLC-P pathway activation. The results obtained by modeling PAI-1 deposition around tumors indicate that matrix-bound PAI-1 is heterogeneously distributed at the tumor periphery and that, at certain spots, the elevated concentrations of matrix-bound PAI-1 needed for cancer cells to undergo the mesenchymal-amoeboid transition can be observed. Matrix-bound PAI-1, as a matricellular protein, could thus represent one of the physiopathological requirements to support metastatic formation.
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Registered trials
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