The Voltage-Gated Sodium Channel Beta4 Subunit Maintains Epithelial Phenotype in Mammary Cells

Research output: Contribution to journalJournal articleResearchpeer-review

  • Adélaïde Doray
  • Roxane Lemoine
  • Marc Severin
  • Stéphanie Chadet
  • Osbaldo Lopez-Charcas
  • Audrey Héraud
  • Christophe Baron
  • Pierre Besson
  • Arnaud Monteil
  • Pedersen, Stine Helene Falsig
  • Sébastien Roger

The SCN4B gene, coding for the NaVβ4 subunit of voltage-gated sodium channels, was recently found to be expressed in normal epithelial cells and down-regulated in several cancers. However, its function in normal epithelial cells has not been characterized. In this study, we demonstrated that reducing NaVβ4 expression in MCF10A non-cancer mammary epithelial cells generated important morphological changes observed both in two-dimensional cultures and in three-dimensional cysts. Most notably, the loss of NaVβ4 induced a complete loss of epithelial organisation in cysts and increased proteolytic activity towards the extracellular matrix. Loss of epithelial morphology was associated with an increased degradation of β-catenin, reduced E-cadherin expression and induction of mesenchymal markers N-cadherin, vimentin, and α-SMA expression. Overall, our results suggest that Navβ4 may participate in the maintenance of the epithelial phenotype in mammary cells and that its downregulation might be a determining step in early carcinogenesis.

Original languageEnglish
Article number1624
JournalCells
Volume10
Issue number7
Number of pages15
ISSN2073-4409
DOIs
Publication statusPublished - 2021

    Research areas

  • epithelial phenotype, epithelial-to-mesenchymal transition, mammary cells, NaVβ4, β-catenin

ID: 275880689