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Article Dans Une Revue Cellular Signalling Année : 2021

Regulatory interplay between Vav1, Syk and β-catenin occurs in lung cancer cells

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Rofia Boudria
  • Fonction : Auteur
Vanessa Laurienté
  • Fonction : Auteur
Antonin Oudar
  • Fonction : Auteur
Souleymane Harouna-Rachidi
  • Fonction : Auteur
Elisabetta Dondi
  • Fonction : Auteur
Christine Le Roy
  • Fonction : Auteur
Laura Gardano
  • Fonction : Auteur
Lionel Guittat
  • Fonction : Auteur

Résumé

Vav1 exhibits two signal transducing properties as an adaptor protein and a regulator of cytoskeleton organization through its Guanine nucleotide Exchange Factor module. Although the expression of Vav1 is restricted to the hematopoietic lineage, its ectopic expression has been unraveled in a number of solid tumors. In this study, we show that in lung cancer cells, as such in hematopoietic cells, Vav1 interacts with the Spleen Tyrosine Kinase, Syk. Likewise, Syk interacts with β-catenin and, together with Vav1, regulates the phosphorylation status of β-catenin. Depletion of Vav1, Syk or β-catenin inhibits Rac1 activity and decreases cell migration suggesting the interplay of the three effectors to a common signaling pathway. This model is further supported by the finding that in turn, β-catenin regulates the transcription of Syk gene expression. This study highlights the elaborated connection between Vav1, Syk and β-catenin and the contribution of the trio to cell migration.

Dates et versions

hal-03874029 , version 1 (27-11-2022)

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Citer

Rofia Boudria, Vanessa Laurienté, Antonin Oudar, Souleymane Harouna-Rachidi, Elisabetta Dondi, et al.. Regulatory interplay between Vav1, Syk and β-catenin occurs in lung cancer cells. Cellular Signalling, 2021, 86, pp.110079. ⟨10.1016/j.cellsig.2021.110079⟩. ⟨hal-03874029⟩
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