MiR‐200c‐3p as a novel genetic marker and therapeutic tool for alopecia areata

Abstract

BackgroundMicroRNAs (miRNAs) are small RNA molecules that regulate gene expression in diverse biological processes. They hold promise as therapeutic candidates for targeting human disease pathways, although our understanding of their gene regulatory mechanism remains incomplete. Alopecia areata (AA) is a prevalent inflammatory ailment distinguished by the infiltration of T cells targeting the anagen‐stage hair follicles. The scarcity of effective remedies for AA may stem from limited understanding regarding its precise cellular mechanism.AimTo investigate and examine the importance and role of the miR‐200c‐3p as a genetic indicator for AA, and its possible impact on disease progression.Subjects and methodsCase‐control study included 65 patients with AA and 65 matched healthy controls. A real‐time PCR technique was used to measure the expression of miR‐200c‐3p for both groups. Bioinformatic tools were used for prediction with genes and gene‐gene interaction, and protein‐protein interaction.ResultsThe expression levels of miR‐200c‐3p were significantly higher in AA patients than in healthy controls. We predicted that miR‐200c‐3p plays a markable role in the development of AA by its effect on the EGFR tyrosine kinase inhibitor resistance pathway.ConclusionWe were able to identify the influence of miR‐200c‐3p on both PLCG1 and RPS6KP1 genes which in turn regulate the EGFR tyrosine kinases resistance pathway that displayed the most substantial increase in activity. Our outcomes shed light on the era of the potential theranostic role of this innovative miRNA in AA.

The role of hsa‐miR‐193a‐5p as an important factor for control of inositol in alopecia areata

“…Hence, the need for further comprehensive and in‐depth exploration and inquiry is paramount to fully comprehending and delineating the multifaceted and intricate role that miRNAs play in the etiology and progression of AA. 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 …”