Roles for GP IIb/IIIa and αvβ3 integrins in MDA-MB-231 cell invasion and shear flow-induced cancer cell mechanotransduction

Zhao, Fenglong; Li, Li; Guan, Liu-Yuan; Yang, Hong; Wu, Chunhui; Liu, Yiyao

doi:10.1016/j.canlet.2013.10.019

Cited by 72 publications

(57 citation statements)

References 57 publications

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“…on May 9, 2018. by guest www.bloodjournal.org From b3 integrin family members (platelet a IIb b 3 , tumor a V b 3 ) in CTC adhesion and invasion under flow conditions, [33][34][35] recent studies revealed that low shear stress upregulated matrix metaloproteinase 2 (MMP-2), MMP-9, VEGF, and a V b 3 integrin, promoting MDA-MB-231 breast carcinoma cell adhesion and invasion, as well as mobilizing both phosphatidylinositol 3-kinase/Akt signaling pathways and NF-kB activation. 36 Using Munc13-4-deficient mice, which present a defect in dense granule secretion but not in a-granule release, Schumacher and colleagues demonstrated that tumor cell-induced platelet aggregation leads to the release of adenosine triphosphate (ATP) stored in dense granules. Then, released ATP binds to the endothelial purinergic P2Y2 receptor, stimulating cancer cell intravasation and metastatic dissemination to the lung, thus demonstrating that ATP secreted from platelets supports platelet-induced tumor cell transendothelial migration and metastatic dissemination 37 ( Figure 1).…”

Section: Platelets and Ctc Invasion/extravasationmentioning

confidence: 99%

Metastasis: new functional implications of platelets and megakaryocytes

Leblanc

Peyruchaud

2016

Blood

184

131

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Platelets are essential components of hemostasis. Due to a plethora of factors released on activation, platelet functions are also connected to tumor growth, notably by acting on angiogenesis. It is now well recognized that major roles of platelets in the poor outcome of cancer patients occurs during hematogenous dissemination of cancer cells. In this review, we describe recent insights into the molecular mechanisms supporting the prometastatic activity of platelets. Platelets have been shown to promote survival of circulating tumor cells (CTCs) in the bloodstream by conferring resistance to the shear stress and attack from natural killer cells. Recently, platelets were found to promote and/or maintain the state of epithelial to mesenchymal transition on CTCs through platelet secretion of transforming growth factor β in response to CTC activation. At a later stage in the metastatic process, platelets promote extravasation and establishment of metastatic cells in distant organs as observed in bone. This particular environment is also the site of hematopoiesis, megakaryocytopoiesis, and platelet production. Increasing the number of megakaryocytes (MKs) in the bone marrow results in a high bone mass phenotype and inhibits skeletal metastasis formation of prostate cancer cells. As a result of their specific location in vascular niches in the bone marrow, MK activity might contribute to the “seed and soil” suitability between CTCs and bone. In conclusion, recent findings have made a great advance in our knowledge on how platelets contribute to the metastatic dissemination of cancer cells and that may support the development of new antimetastasis therapies.

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Section: Platelets and Ctc Invasion/extravasationmentioning

confidence: 99%

Metastasis: new functional implications of platelets and megakaryocytes

Leblanc

Peyruchaud

2016

Blood

184

131

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“…Integrins transduce signals from the extracellular environment to the cell interior; in this way, changes in the concentrations of key signaling molecules in the plasma are communicated to the cell. In addition, integrins have more recently been recognized as sensors of the mechanical environment surrounding the cell, which also results in changes in intracellular signal transduction pathways (139,147). In addition, integrins receive intracellular signals that regulate their ligand-binding affinity, fine-tuning the communication between the cell FIG.…”

Section: Mechanosensors In the Aortic Valve Endotheliummentioning

confidence: 99%

Shear-Sensitive Genes in Aortic Valve Endothelium

Esmerats

Heath

2016

Antioxidants & Redox Signaling

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Significance: Currently, calcific aortic valve disease (CAVD) is only treatable through surgical intervention because the specific mechanisms leading to the disease remain unclear. In this review, we explore the forces and structure of the valve, as well as the mechanosensors and downstream signaling in the valve endothelium known to contribute to inflammation and valve dysfunction. Recent Advances: While the valvular structure enables adaptation to dynamic hemodynamic forces, these are impaired during CAVD, resulting in pathological systemic changes. Mechanosensing mechanisms-proteins, sugars, and membrane structures-at the surface of the valve endothelial cell relay mechanical signals to the nucleus. As a result, a large number of mechanosensitive genes are transcribed to alter cellular phenotype and, ultimately, induce inflammation and CAVD. Transforming growth factor-b signaling and Wnt/b-catenin have been widely studied in this context. Importantly, NADPH oxidase and reactive oxygen species/reactive nitrogen species signaling has increasingly been recognized to play a key role in the cellular response to mechanical stimuli. In addition, a number of valvular microRNAs are mechanosensitive and may regulate the progression of CAVD. Critical Issues: While numerous pathways have been described in the pathology of CAVD, no treatment options are available to avoid surgery for advanced stenosis and calcification of the aortic valve. More work must be focused on this issue to lead to successful therapies for the disease. Future Directions: Ultimately, a more complete understanding of the mechanisms within the aortic valve endothelium will lead us to future therapies important for treatment of CAVD without the risks involved with valve replacement or repair. Antioxid. Redox Signal. 25, 401-414.

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“…Cell invasion assay As previously described, 25 MCF-7 cells were trypsinized and resuspended in culture medium containing 2% FBS. A total 1 × 10 5 cells that were pretreated with RS102895, U0126, LiCl or LY294002 were seeded into the Matrigel (BD Biosciences, San Diego, CA, USA)-coated transwell upper chambers (pore size of 8.0 μm), and medium containing 10% FBS was added to the lower chamber.…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

MCP-1-induced ERK/GSK-3β/Snail signaling facilitates the epithelial–mesenchymal transition and promotes the migration of MCF-7 human breast carcinoma cells

Lü

Chen

et al. 2016

Cell Mol Immunol

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Monocyte chemoattractant protein-1 (MCP-1) is a chemotactic cytokine that can bind to its receptor cysteine-cysteine chemokine receptor 2 (CCR2) and plays an important role in breast cancer cell metastasis. However, the molecular mechanisms underlying MCP-1-induced alterations in cellular functions during tumor progression are poorly understood. Here, we showed that MCP-1 stimulated the epithelial-mesenchymal transition (EMT) and induced the tumorigenesis of breast cancer cells by downregulating E-cadherin, upregulating vimentin and fibronectin, activating matrix metallopeptidase-2 (MMP-2), and promoting migration and invasion. Moreover, MCP-1 treatment reduced glycogen synthase kinase-3β (GSK-3β) activity via the MEK/ERK-mediated phosphorylation of serine-9 in MCF-7 cells. The inhibition of MEK/ERK by U0126 attenuated the MCP-1-induced phosphorylation of GSK-3β and decreased the expression of Snail, an EMT-related transcription factor, leading to the inhibition of MCF-7 cell migration and invasion. Inactivation of GSK-3β by LiCl (lithium chloride) treatment notably increased MMP-2 activity, vascular endothelial growth factor expression and EMT of MCF-7 cells. These findings revealed that MCP-1-induced EMT and migration are mediated by the ERK/GSK-3β/Snail pathway, and identified a potential novel target for therapeutic intervention in breast cancer. Cellular & Molecular Immunology

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Roles for GP IIb/IIIa and αvβ3 integrins in MDA-MB-231 cell invasion and shear flow-induced cancer cell mechanotransduction

Cited by 72 publications

References 57 publications

Metastasis: new functional implications of platelets and megakaryocytes

Metastasis: new functional implications of platelets and megakaryocytes

Shear-Sensitive Genes in Aortic Valve Endothelium

MCP-1-induced ERK/GSK-3β/Snail signaling facilitates the epithelial–mesenchymal transition and promotes the migration of MCF-7 human breast carcinoma cells

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