- •miR- 185–5p was downregulated in responder patients relative to non-responders.
- •MAPK signaling was predicted as an important pathway in interferon-beta signaling.
- •miR-185–5p can be considered as a novel biomarker for therapy response.
Multiple sclerosis (MS) is an inflammatory autoimmune disease characterized by neurodegeneration in the CNS. Interferon-beta (IFN-β) is an FDA-approved drug used as the first-line treatment for relapse-remitting multiple sclerosis (RRMS). The exact mechanism of IFN-β during the treatment of RRMS still remains unknown. Recently, many studies have shifted towards the role of miRNAs in the treatment of MS patients.
Herein, the expression level of miR-185–5p and miR-320a has been evaluated in order to candidate them as novel biomarkers for monitoring the response to IFN-β therapy. For this purpose, one-hundred whole blood samples from patients with RRMS were collected, consisting of 50 responders and 50 non-responders to IFN-β therapy. To predict the possible molecular mechanisms of IFN-β and highlight the role of these miRNAs, in silico analysis was applied to enrich the signaling pathways which may be involved based on the target genes of miR-185–5p and miR-320a.
It is identified that the differentially expressed miR-185–5p was statistically significant between the two treated groups with IFN-β. Furthermore, MAPK signaling pathway was suggested as the main non-canonical pathway involved in IFN-β therapy.
miR-185–5p could be considered as a novel biomarker for monitoring the response to IFN-β therapy.
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Published online: June 07, 2020
Accepted: June 3, 2020
Received in revised form: May 27, 2020
Received: September 3, 2019
© 2020 Elsevier B.V. All rights reserved.