Positive regulation of migration and invasion by vasodilator-stimulated phosphoprotein via Rac1 pathway in human breast cancer cells
Guoge Han,Biao Fan,Yimin Zhang,Xuan Zhou,Yongping Wang,Huimin Dong,Yun Wei,Shengrong Sun,Mingbo Hu,Jingwei Zhang,Lei Wei +10 more
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TLDR
The data showed that the higher expression level of VASP contributed to a higher invasive migration capacity of human breast cancer cells which was controlled by the Rac1 pathway.Abstract:
This study aimed to investigate the role of the cytoskeleton-associated protein vasodilator-stimulated phosphoprotein (VASP) on the migration and invasion of human breast cancer cells and its relationship to Rac1 which is a member of the Rho family and has been found to be implicated in tumorigenesis, invasion and metastasis. We detected the mRNA and protein expression levels of VASP and Rac1 of the non-invasive breast cancer cell line MCF-7 as well as the invasive cell line MDA-MB-231 by RT-PCR and Western blotting. GST pull-down assay was used to examine the activity of Rac1. Accordingly, the cell invasive migration ability was analyzed in a wound-healing assay (2D) and transwell assays (3D migration and invasion). We then used VASP-siRNA to inhibit the expression of VASP in breast cancer cells in order to study the relationship between the VASP expression level and the invasive migration ability of breast cancer cells. Rac1-siRNA was used to decrease the expression of Rac1, and observe its effect on the VASP expression level together with the migration and invasion ability of MCF-7 and MDA-MB-231 cells. Our results revealed that the invasive breast cancer cell line MDA-MB-231 showed a higher Rac1 activity and VASP expression level compared with the non-invasive MCF-7. Inhibition of Rac1 or VASP by siRNA, respectively, decreased the migration and invasion ability of breast cancer cells and the transfection of Rac1 siRNA-mediated reduction of VASP expression at mRNA and protein levels. Collectively, our data showed that the higher expression level of VASP contributed to a higher invasive migration capacity of human breast cancer cells which was controlled by the Rac1 pathway.read more
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Hypoxic Tumor Cell Modulates Its Microenvironment to Enhance Angiogenic and Metastatic Potential by Secretion of Proteins and Exosomes
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TL;DR: In this article, the authors observed that tumor cells produce a secretion that modifies their microenvironment to facilitate tumor angiogenesis and metastasis under hypoxia, and the secreted proteins were predominantly cytoplasmic and membrane proteins.
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G protein-coupled receptors stimulation and the control of cell migration.
Mathieu Cotton,Audrey Claing +1 more
TL;DR: The role of GPCR mediated signal transduction and their importance in the regulation of actin remodeling leading to cell migration are reviewed.
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Characterization of EHop-016, Novel Small Molecule Inhibitor of Rac GTPase
Brenda L. Montalvo-Ortiz,Linette Castillo-Pichardo,Eliud Hernandez,Tessa Humphries-Bickley,Alina De La Mota-Peynado,Luis A. Cubano,Cornelis P. Vlaar,Suranganie Dharmawardhane +7 more
TL;DR: It is demonstrated that EHop-016 inhibits Rac activity in the MDA-MB-435 metastatic cancer cells that overexpress Rac and exhibits high endogenous Rac activity, and holds promise as a targeted therapeutic agent for the treatment of metastatic cancers with high Rac activity.
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Cell biology of the movement of breast cancer cells: intracellular signalling and the actin cytoskeleton.
TL;DR: This review of recent literature focuses on aspects of cell biology related to motility and metastasis, and suggests some directions for future breast cancer research.
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Hypoxia-induced up-regulation of VASP promotes invasiveness and metastasis of hepatocellular carcinoma.
Zhikui Liu,Yufeng Wang,Changwei Dou,Meng Xu,Liankang Sun,Liang Wang,Bowen Yao,Qing Li,Wei Yang,Kangsheng Tu,Qingguang Liu +10 more
TL;DR: VASP was defined as an oncogene of HCC pathogenesis and metastasis with the potential to serve as a prognostic biomarker after a variety of hypoxia-induced molecular mechanisms contributed to the upregulation of VASP at transcriptional and post-transcriptional levels.
References
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Actin-based motility: stop and go with Ena/VASP proteins
TL;DR: Although biochemical mechanisms have emerged depicting Ena/VASP proteins as enhancers of actin filament formation, increasing evidence suggests that these proteins have inhibitory functions in integrin regulation, cell motility and axon guidance.
Journal ArticleDOI
Translocation of cortactin to the cell periphery is mediated by the small GTPase Rac1
TL;DR: Evidence is provided that the intracellular localization of the actin binding protein cortactin, a Src kinase substrate, is regulated by the activation of Rac1, and this translocation is blocked by expression of dominant negative Rac1N17.
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Rac1-deficient macrophages exhibit defects in cell spreading and membrane ruffling but not migration
Claire M. Wells,Marita J. Walmsley,Steen K.T. Ooi,Victor L. J. Tybulewicz,Anne J. Ridley,Anne J. Ridley +5 more
TL;DR: It is shown that mouse bone marrow-derived macrophages express Rac1, low levels of Rac2 but not Rac3, and that Rac1 is primarily responsible for regulating cell morphology, contributes to membrane ruffling, but is not required for migration.
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Rac1 mediates type I collagen-dependent MMP-2 activation. role in cell invasion across collagen barrier.
Yuzheng Zhuge,Jiahua Xu +1 more
TL;DR: Evidence is provided that Rac1, one member of Rho-related small GTPases, is a mediator of MMP-2 activation in HT1080 fibrosarcoma cells cultured in three-dimensional collagen gel and that MMP -2 activation is required for Rac1-promoted cell invasion through collagen barrier.
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Expression of seven main Rho family members in gastric carcinoma.
TL;DR: The mRNA expression levels of RhoA and Rac1 in gastric cancer tissue specimens were significantly higher than those in the adjacent non-tumorous tissue specimens, and this indicates that Rho a and Rac 1 may play important roles in the carcinogenesis and progression of gastric carcinoma.