How integrins control breast biology

Glukhova, Marina A.; Streuli, Charles

doi:10.1016/j.ceb.2013.06.010

Cited by 57 publications

(55 citation statements)

References 88 publications

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“…We found a significant reduction in p(Tyr1510) levels of the integrin β4 subunit in luminal cells (Paper 2 Fig.3c). Integrin β4 influences laminin signal transduction, supporting the notion that the laminin-mediated signaling associated with HMEC differentiation is diminished with age (Glukhova & Streuli 2013;Streuli & Akhtar 2009;Li et al 2003). Proliferative and migratory behaviours supported by fibronectin and collagen I (Carey et al 2017) are similarly downregulated in older HMEC.…”

Section: Contextual Response Of Cells In An Ageing Microenvironment Isupporting

confidence: 48%

“…The sensing of the cellular microenvironment comprises cell-cell and cell-ECM interactions, as well as interactions with soluble and tensile factors (Glukhova & Streuli 2013). The microenvironment has 1) chemical properties conveyed through the ligand-receptor transition; 2) physical properties including the stiffness and elasticity of the tissue transferred through mechanoreceptors being pushed and pulled and 3)…”

Section: Mammary Microenvironmentmentioning

confidence: 99%

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Microsphere cytometry to interrogate microenvironment-dependent cell signaling

et al. 2017

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2018Avhandling for graden philosophiae doctor (ph.d.)Dato for disputas: 06.04.18Trykk:Skipnes Kommunikasjon / Universitetet i Bergen Materialet i denne publikasjonen er omfattet av åndsverkslovens bestemmelser. Tittel:The effects of ageing on microenvironment-contextual epithelial cell signalling Rein Aasland, for valuable insight on academic writing, and for pointing out, as did James, when my words became self-indulgent fun and flowers. Mark LaBarge, for taking me into his lab, and letting me partake in that which concerns absolutely everyone: ageing. To Martha Stampfer for allowing me to poke around in her human cell resources biobank. To James Garbe for being an incredibly sympathetic guy with the most convenient knowledge up his sleeve.I would like to thank my mother Nina-Mamma for never curbing her enthusiasm for tiny biology when I brought home science homework, and my father Ulf for being genuinely impressed with pretty much everything I didincluding when I did it badly. I need to thank my boyfriend, Lars, for meticulous proofreading of the manuscript, and for continuously encouraging me to put my academic whims into writing. I want to point out that Iren Abrahamsen did substantial preliminary work for the microsphere cytometry method. I need to to thank my medical doctor office mates, Gry and Kjersti for valuable insights from the clinical realm where lab rats never go, to remind me who we're doing this for in the first place. Thanks to Sissel for being that steady rock in the corner stall of the lab where PhDs and postdocs fly by. I would like to thank the girls in the lab for taking up the fight against cancer cell Fråtse-Frida, and winning it. Finally, I would like to thank the Cancer Society, VilVite, CCBIO and Forskningsdagene for giving me trust, whether it was to develop flow cytometry protocols or popular science shows, or to interrogate the microenvironment I would like thank just anyone else in the lab and the general world who is interested and willing to contemplate big ideas such as the purpose of being. And at last, every single nerd: nerdy boys and nerdy girls. pathway activation levels in HMEC are attenuated with age, and that the diminished signaling magnitude in HMEC from ageing women correlated with reduced probability of activating oncogene-induced senescence.Our results suggest that attenuated cell signaling response may reduce the likelihood of activating oncogene induced senescence, for cells in ageing women. We hypothesize this is the result of age-related changes to the microenvironment that support age-emergent cellular phenotypes with increased cancer susceptibility.

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Section: Contextual Response Of Cells In An Ageing Microenvironment Isupporting

confidence: 48%

Section: Mammary Microenvironmentmentioning

confidence: 99%

Microsphere cytometry to interrogate microenvironment-dependent cell signaling

et al. 2017

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“…The array included the most abundant ECM proteins that are present under physiological conditions in the basal membrane in breast tissue, such as collagen I, IV, fibronectin and laminin [34]. We found that NEDD9 depletion lead to a significant decrease in adhesion to laminin, collagen I and IV (Fig.2A).…”

Section: Resultsmentioning

confidence: 87%

Prometastatic NEDD9 Regulates Individual Cell Migration via Caveolin-1–Dependent Trafficking of Integrins

Kozyulina

Loskutov

Kozyreva

et al. 2015

Molecular Cancer Research

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The dissemination of tumor cells relies on efficient cell adhesion and migration, which in turn depends upon endocytic trafficking of integrins. In the current work, it was found that depletion of pro-metastatic protein, NEDD9, in breast cancer (BC) cells results in a significant decrease in individual cell migration due to impaired trafficking of ligand-bound integrins. NEDD9 deficiency does not affect the expression or internalization of integrins but heightens caveolae-dependent trafficking of ligand-bound integrins to early endosomes. Increase in mobility of ligand-bound integrins is concomitant with an increase in tyrosine phosphorylation of caveolin-1 (CAV1) and volume of CAV1-vesicles. NEDD9 directly binds to CAV1 and co-localizes within CAV1 vesicles. In the absence of NEDD9, the trafficking of ligand-bound integrins from early to late endosomes is impaired, resulting in a significant decrease in degradation of ligand/integrin complexes and an increase in recycling of ligand-bound integrins from early endosomes back to the plasma membrane without ligand disengagement, thus leading to low adhesion and migration. Re-expression of NEDD9 or decrease in the amount of active, tyrosine 14 phosphorylated (Tyr14) CAV1 in NEDD9 depleted cells rescues the integrin trafficking deficiency and restores cellular adhesion and migration capacity. Collectively, these findings indicate that NEDD9 orchestrates trafficking of ligand-bound integrins through the attenuation of CAV1 activity.

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“…Integrins signaling is thus involved in the establishment of the apico-basal polarity (e.g. apical side speciation) of MECs and lumen formation during pregnancy, enables PRL signaling through its effectors Jak2 and Stat5 to activate milk protein genes during lactation, as well as remodeling of the mammary tissue during involution [35]. Moreover, the composition and stiffness of the BM change during MG development according to the variations in the ratio of the mammary cell types.…”

Section: Functional Anatomy Of the Lactating Breastmentioning

confidence: 99%

“…Moreover, the composition and stiffness of the BM change during MG development according to the variations in the ratio of the mammary cell types. Therefore, there is a critical interdependency of tissue architecture and cell fate for the spatio-temporal regulation of both mammary development and function [35]. Thus, by transducing both biochemical (survival, differentiation and functional) and biophysical signals (changes in cell shape or membrane tension through cytoskeletal changes), integrins determine the fate of MECs [35,36].…”

Section: Functional Anatomy Of the Lactating Breastmentioning

confidence: 99%