Is β-catenin neutralization cross-involved in the mechanisms mediated by natalizumab action?

M. Galuppo, E. Mazzon, S. Giacoppo, O. Bereshchenko, S. Bruscoli, C. Riccardi, P. Bramanti

Research output: Contribution to journalArticlepeer-review

Abstract

Aberrant activation of Wnt/β-catenin signaling pathway is commonly associated to cancer development. However, molecular mechanisms controlling Wnt/β-catenin signaling pathway have been clarified only in part. Here, we show that β-catenin is differently modulated in patients with multiple sclerosis (MS), displaying that different pharmacological treatments used for clinical MS management cause different nuclear expression levels of β-catenin. Proteins extracted by peripheral blood mononuclear cells were assessed to evaluate the western blot expression levels of β-catenin. Analyzing our results, we realized that β-catenin is totally inhibited by Natalizumab and could have a role in MS management. This could offer new promising studies focused on the possible therapeutic control of β-catenin translocation.

Original languageEnglish
Pages (from-to)990-993
Number of pages4
JournalCurrent Molecular Medicine
Volume15
Issue number10
Publication statusPublished - Dec 1 2015

Keywords

  • First diagnosis patients
  • Interferon-beta
  • Natalizumab
  • Neurodegenerative disease
  • Relapsing/remitting multiple sclerosis
  • Wnt/β-catenin pathway

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Molecular Medicine

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