CdGAP is a talin-binding protein and a target of TGF-β signaling that promotes HER2-positive breast cancer growth and metastasis

He, Yi; Goyette, Marie-Anne; Chapelle, Jennifer; Boufaied, Nadia; Rahbani, Jalal Al; Schonewolff, Maribel; Danek, Eric I.; Muller, William J.; Labbé, David P.; Côté, Jean‐François; Lamarche-Vane, Nathalie

doi:10.1016/j.celrep.2023.112936

Cited by 3 publications

(2 citation statements)

References 85 publications

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“…Moreover, depletion of talin1 in colorectal cancer cells inhibited the expression of EMT marker vimentin and elevated E-cadherin levels [122]. In another EMT-driving mechanism, CdGAP was shown to bind talin and activate integrins in a TGFβ-dependent manner, promoting cell adhesion and TGFβ-induced EMT [123].…”

Section: Talins and Integrins In The Epithelial-mesenchymal Transitionmentioning

confidence: 99%

Review on the molecular mechanism of talin- and integrin-dependent cancer invasion

Baster¹,

Russell²,

Rajfur³

2023

Preprint

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Cancer is the second most common cause of death in the world, representing one of the main economic burden in healthcare and research. The effort of research has been mainly focused on limiting of the growth of a localized tumor but most recently there is more attention focused on limiting the spreading of the cancer via invasion and metastasis. The signaling pathways behind these two processes, share many molecules with physiological pathways regulating cell adhesion and migration, and moreover, adhesion and migration processes themselves underlie tumor capabilities for invasion.In this work we reviewed the latest Literature about cancer development and invasion, and their connection to proteins regulating cell migration and adhesion, with a specific focus on talins and integrins. First we analyzed cancer epidemiology and risk factors behind carcinogenesis. Next, we concentrated on molecules regulating adhesion and migration in cells, and reviewed the latest finding describing molecular mechanisms of talin- and integrin-dependent cancer invasion. Finally, we summarized the most recent development and approaches to anti-cancer therapies, with particular focus on cell migration-related therapies.

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Section: Talins and Integrins In The Epithelial-mesenchymal Transitionmentioning

confidence: 99%

Review on the molecular mechanism of talin- and integrin-dependent cancer invasion

Baster¹,

Russell²,

Rajfur³

2023

Preprint

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“…Migration assays were performed and analysed as previously described (17). 100,000 cells were resuspended in serum-free medium and plated on the top chamber (24-well transwell insert, Falcon: 353097).…”

Section: Migration Assaymentioning

confidence: 99%

Biallelic variants inARHGAP19cause a motor-predominant neuropathy with asymmetry and conduction slowing

Dominik,

Efthymiou,

Record

et al. 2024

Preprint

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Charcot-Marie-Tooth Disease is a clinically and genetically heterogeneous group of hereditary neuropathies, with over 100 causative genes identified to date. Despite progress in genetic sequencing, around a quarter of patients remain unsolved. Through international collaborations, we identified 16 recessive variants in Rho GTPase activating protein 19 (ARHGAP19) causing motor-predominant neuropathy with conduction slowing in 25 individuals from 20 unrelated multi-ancestry families. ARHGAP19 is a GTPase-activating protein with activity towards RhoA. In vitro biochemical assays revealed that variants located within the GAP domain cause loss of GAP activity. iPSc-derived motor neurons exhibited 50% knockdown of ARHGAP19 protein. In vivo genetic perturbations of the Drosophila melanogaster ARHGAP19 ortholog RhoGAP54D reduced self-driven locomotor activity and startle responses to visual stimuli. Zebrafish loss-of-function models similarly exhibited movement deficits, coupled with increased motor neuron axonal branching but shorter caudal primary motor neurons. Together, these findings establish ARHGAP19 as a novel cause of early-onset neuropathy through a loss-of-function mechanism.

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Crosstalk between TGF-β and EGF receptors via direct phosphorylation

Moustakas

2024

Journal of Cell Biology

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CdGAP is a talin-binding protein and a target of TGF-β signaling that promotes HER2-positive breast cancer growth and metastasis

Cited by 3 publications

References 85 publications

Review on the molecular mechanism of talin- and integrin-dependent cancer invasion

Review on the molecular mechanism of talin- and integrin-dependent cancer invasion

Biallelic variants inARHGAP19cause a motor-predominant neuropathy with asymmetry and conduction slowing

Crosstalk between TGF-β and EGF receptors via direct phosphorylation

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