Antibody-Induced Activation of β1 Integrin Receptors Stimulates cAMP-Dependent Migration of Breast Cells on Laminin-5

Plopper, George E.; Huff, Janice L.; Rust, Will; Schwartz, Martin A.; Quaranta, Vito

doi:10.1006/mcbr.2001.0267

Cited by 15 publications

(12 citation statements)

References 22 publications

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“…The increased transcription of MTSS1 could also function to mitigate the significantly reduced expression of two different MHC class I genes, as observed among the EPH individuals. It is now well established that the down-regulation of MHC class I genes is tightly associate to cell metastasis, as this process can greatly facilitate the concealment of the tumour cells from T cell-mediated immune response 53, 54 .…”

Section: Resultsmentioning

confidence: 99%

Impacts of Early Life Stress on the Methylome and Transcriptome of Atlantic Salmon

Moghadam

Robinson

Andersen

et al. 2017

Sci Rep

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Exposure to environmental stressors during early-life stages can change the rate and timing of various developmental processes. Epigenetic marks affecting transcriptional regulation can be altered by such environmental stimuli. To assess how stress might affect the methylome and transcriptome in salmon, fish were treated using cold-shock and air-exposure from the eye-stage until start-feeding. The fish were either stressed prior to hatching (E), post-hatching (PH), pre- and post-hatching (EPH) or not stressed (CO). Assessing transcriptional abundances just prior to start feeding, E and PH individuals were found to have modified the expression of thousands of genes, many with important functions in developmental processes. The EPH individuals however, showed expression similar to those of CO, suggesting an adaptive response to extended periods of stress. The methylome of stressed individuals differed from that of the CO, suggesting the importance of environment in shaping methylation signatures. Through integration of methylation with transcription, we identified bases with potential regulatory functions, some 10s of kb away from the targeted genes. We then followed fish growth for an additional year. Individuals in EPH showed superior growth compared to other treatment groups, highlighting how stress can potentially have long-lasting effects on an organism’s ability to adapt to environmental perturbations.

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Section: Resultsmentioning

confidence: 99%

Impacts of Early Life Stress on the Methylome and Transcriptome of Atlantic Salmon

Moghadam

Robinson

Andersen

et al. 2017

Sci Rep

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“…41,42 The tendency of laminin-binding integrins to activate Rac1 43,44 strongly suggests that CD151 sustains Rac1 activity by reinforcing the function of laminin-binding integrins. Laminin-binding integrins induce cAMP signaling 45,46 ; and in microvascular ECs, cAMP primarily enhances Rac1 and subsequently reduces RhoA activity. 47 When CD151 is absent, the reduced cAMP/PKA signaling causes the down-regulation of Rac1 and then indirectly leads to the up-regulation of RhoA, given the antagonism between Rac1 and RhoA signaling.…”

mentioning

confidence: 99%

Tetraspanin CD151 maintains vascular stability by balancing the forces of cell adhesion and cytoskeletal tension

Zhang

Michaelson

Moshiach

et al. 2011

Blood

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IntroductionTetraspanin CD151 forms stable and stoichiometric associations with laminin-binding integrins and regulates cellular functions, such as cell-matrix adhesion strengthening, epithelial cell-cell adhesion, and cell migration. [1][2][3][4] In endothelial cells (ECs), cell surface CD151 is localized at basolateral surfaces and forms tetraspanin-enriched microdomain (TEM) with other tetraspanins and integrins. [5][6][7] The CD151-containing TEM on ECs is critical for the proper function of adhesion proteins, such as ICAM-1 and VCAM-1, and is needed for the transendothelial migration of lymphocytes. 8 In addition, CD151 regulates EC migration 5,6,9 and promotes vascular morphogenesis both in vitro 5,9,10 and in vivo. 11 Pathologic angiogenesis becomes deficient in CD151-knockout mice. 9 However, the mechanism by which CD151 regulates various vascular functions remains largely unknown. Mechanistic studies from epithelial and carcinoma cells indicate that CD151-␣3␤1 integrin complex regulates cell-cell adhesion, probably by organizing or stabilizing cell-cell junctional complexes. 12,13 CD151 overexpression leads to PKC-and Cdc42-dependent reorganization of actin cytoskeleton, 2 whereas CD151 silencing results in higher RhoA activity and more stress fiber formation, 13 suggesting that CD151 modulates the epithelial cytoskeletal machinery. In ECs, CD151 up-regulates eNOS, Akt, and Rac activities 9,11 and promotes TEM-metalloprotease association. 14 Endothelial cell-cell and cell-matrix adhesions are required for the formation and maintenance of blood vessels. 15 VE-cadherin is linked to actin cytoskeleton by ␣-, ␤-, ␥-, and p120-catenin to form adherens junctions (AJs). 16 Integrins bridge intracellular actin fibers to extracellular matrices to anchor ECs to the basement membrane. 17 Rho small GTPase-mediated cytoskeletal reorganizations are also important for blood vessels. For example, Rac1-and Cdc42-dependent protrusions are essential for vessel structure formation and integrity, whereas RhoA-mediated retraction destabilizes angiogenic vessels and induces regression. [18][19][20] Rho GTPases and cadherin-mediated cell-cell adhesion are mutually regulated. Activation of RhoA induces the disassembly of cell-cell adhesion via myosin II-mediated cytoskeletal tension, 21 whereas AJs inhibit RhoA signaling by recruiting p190Rho GAP into the junctions. 22 Herein we found that the loss of CD151 expression disrupts endothelial stability in vascular morphogenesis and other vascular events. At the molecular level, lack of CD151 leads to decreased cAMP/PKA signaling and deregulated Rac1 and RhoA signaling. At the cellular level, attenuated endothelial cell-cell and cell-matrix adhesions coupled with elevated cytoskeletal tension directly destabilize endothelial structure. Our study emphasizes that CD151 balances cell adhesion and cytoskeletal tension in ECs to maintain vascular stability. Methods Reagents, animals, and cell cultureInformation regarding reagents, animals, and cell culture is provided in supplemental Met...

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“…To resolve which pathways mediate HGF-stimulated AREG release, specific inhibitors of growth factor signaling pathways enhanced by integrins, including MAPK, PKA, Src, and PI3K (7,(35)(36)(37)(38)(39), and the classical PKC pathway, were tested for their ability to block AREG secretion in response to HGF. As shown in Fig.…”

Section: D7 Cells As Shown Inmentioning

confidence: 99%

Integrin α6β4 Promotes Autocrine Epidermal Growth Factor Receptor (EGFR) Signaling to Stimulate Migration and Invasion toward Hepatocyte Growth Factor (HGF)

Carpenter

Chen

Knifley

et al. 2015

Journal of Biological Chemistry

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Background: Integrin ␣6␤4 is overexpressed in pancreatic cancer and enhances invasion. Results: Integrin ␣6␤4 coordinately up-regulates AREG, EREG, and MMP1 through DNA demethylation and NFAT5 that in turn enhances HGF-mediated invasion. Conclusion: Integrin ␣6␤4 stimulates HGF-dependent invasion through autocrine EGFR signaling. Significance: HGF-stimulated invasion is dependent on autocrine EGFR signaling, thus implicating why EGFR inhibitors are effective in a complex tumor microenvironment.

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Antibody-Induced Activation of β1 Integrin Receptors Stimulates cAMP-Dependent Migration of Breast Cells on Laminin-5

Cited by 15 publications

References 22 publications

Impacts of Early Life Stress on the Methylome and Transcriptome of Atlantic Salmon

Impacts of Early Life Stress on the Methylome and Transcriptome of Atlantic Salmon

Tetraspanin CD151 maintains vascular stability by balancing the forces of cell adhesion and cytoskeletal tension

Integrin α6β4 Promotes Autocrine Epidermal Growth Factor Receptor (EGFR) Signaling to Stimulate Migration and Invasion toward Hepatocyte Growth Factor (HGF)

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