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.
Keywords: Relapsing/remitting multiple sclerosis, first diagnosis patients, Wnt/β-catenin pathway, natalizumab,
interferon-beta, neurodegenerative disease.
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