Rac1 Mediates Type I Collagen-dependent MMP-2 Activation

Zhuge, Yuzheng; Xu, Jiahua

doi:10.1074/jbc.m010190200

Cited by 160 publications

(122 citation statements)

References 66 publications

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“…The pro-invasive activity of Rac1 is associated with enhanced expression and secretion of MMPs (22)(23)(24). Zhang et al (23) reported that extracellular ATP facilitates the invasion of prostate cancer cells through the activation of Rac1 and Cdc42 and the upregulation of MMP-3 and MMP-13.…”

Section: Discussionmentioning

confidence: 99%

Bergamottin, a natural furanocoumarin abundantly present in grapefruit juice, suppresses the invasiveness of human glioma cells via inactivation of Rac1 signaling

et al. 2017

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Abstract. The aim of the present study was to explore the effect of bergamottin, a natural furanocoumarin obtained from grapefruit juice, on the invasiveness of human glioma cells. The results revealed that treatment with bergamottin for 48 h significantly inhibited wound-healing migration and Matrigel invasion of human glioma cells, compared with untreated cells (P<0.05). Bergamottin treatment caused a significant decrease in the expression and secretion of matrix metalloproteinase (MMP)-9 in glioma cells compared with untreated cells (P<0.05). A Rac1-GTP pull-down assay demonstrated that bergamottin-treated glioma cells had a significantly decreased level of active Rac1-GTP compared with untreated cells (P<0.05). However, bergamottin had no significant effect on cell division cycle 42 activity. Expression of constitutively activated Rac1 almost completely restored the migration and invasion of bergamottin-treated glioma cells. In addition, bergamottin-induced downregulation of MMP-9 was prevented by exogenous activated Rac1. The results of the present study demonstrated that bergamottin exhibits anti-invasive activity in human glioma cells through the inactivation of Rac1 and downregulation of

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Section: Discussionmentioning

confidence: 99%

Bergamottin, a natural furanocoumarin abundantly present in grapefruit juice, suppresses the invasiveness of human glioma cells via inactivation of Rac1 signaling

et al. 2017

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“…It is tempting to speculate that Rac is degraded by this antizymeproteasome pathway, because no shift in molecular mass is detectable after precipitation of the activated Rac. Moreover, one can say that cells may possess a mechanism for rapid degradation of Rac to prevent the effects of prolonged activation of the GTPase (11,29). It has previously been reported that the levels of Rho decrease after ADP ribosylation by the C3 exoenzyme from Clostridium botulinum (19).…”

Section: Discussionmentioning

confidence: 99%

Proteasomal Degradation of Cytotoxic Necrotizing Factor 1-Activated Rac

Lerm

Pop

Fritz³

et al. 2002

Infect Immun

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“…The involvement of Rac in cell invasion has been established in several experimental systems (59 -62). The overexpression of activated Rac1 promotes the invasion of some carcinoma cell lines in collagen (59,63), whereas the dominant negative forms of Rac1 inhibit leptinstimulated cell invasion in collagen gels (60), implicating Rac1-dependent pathways in epithelial cell invasion. However, activated Rac also promotes enhanced cell-cell junction assembly in MDCK cells (64), inhibiting their dispersal in response to HGF (65,66).…”

Section: Mek1-dependent Signals Synergize With Crkii To Promote the Lmentioning

confidence: 99%

Crk Synergizes with Epidermal Growth Factor for Epithelial Invasion and Morphogenesis and Is Required for the Met Morphogenic Program

Lamorte¹,

Rodrigues²,

Naujokas³

et al. 2002

Journal of Biological Chemistry

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Activation of the Met receptor tyrosine kinase through its ligand, hepatocyte growth factor, stimulates cell spreading, cell dispersal, and the inherent morphogenic program of various epithelial cell lines. Although both hepatocyte growth factor and epidermal growth factor (EGF) can activate downstream signaling pathways in Madin-Darby canine kidney epithelial cells, EGF fails to promote the breakdown of cell-cell junctional complexes and initiate an invasive morphogenic program. We have undertaken a strategy to identify signals that synergize with EGF in this process. We provide evidence that the overexpression of the CrkII adapter protein complements EGF-stimulated pathways to induce cell dispersal in two-dimensional cultures and cell invasion and branching morphogenesis in three-dimensional collagen gels. This finding correlates with the ability of CrkII to promote the breakdown of adherens junctions in stable cell lines and the ability of EGF to stimulate enhanced Rac activity in cells overexpressing CrkII. We have previously shown that the Gab1-docking protein is required for branching morphogenesis downstream of the Met receptor. Consistent with a role for CrkII in promoting EGF-dependent branching morphogenesis, the binding of Gab1 to CrkII is required for the branching morphogenic program downstream of Met. Together, our data support a role for the CrkII adapter protein in epithelial invasion and morphogenesis and underscores the importance of considering the synergistic actions of signaling pathways in cancer progression.Epithelial morphogenesis is essential for normal embryonic development and involves proliferation, migration, cellular invasion, turnover of surrounding extracellular matrix, and the deposition of newly synthesized extracellular matrix (1). Several growth factors stimulate the morphogenic program of epithelial cells.

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Rac1 Mediates Type I Collagen-dependent MMP-2 Activation

Cited by 160 publications

References 66 publications

Bergamottin, a natural furanocoumarin abundantly present in grapefruit juice, suppresses the invasiveness of human glioma cells via inactivation of Rac1 signaling

Bergamottin, a natural furanocoumarin abundantly present in grapefruit juice, suppresses the invasiveness of human glioma cells via inactivation of Rac1 signaling

Proteasomal Degradation of Cytotoxic Necrotizing Factor 1-Activated Rac

Crk Synergizes with Epidermal Growth Factor for Epithelial Invasion and Morphogenesis and Is Required for the Met Morphogenic Program

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