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microRNA-205-5p (miR-205-5p) is a highly conserved, small non-coding RNA that serves as a pivotal post-transcriptional regulator of gene expression across various tissues [2, 7]. It primarily functions by binding to the 3' untranslated regions (UTRs) of target messenger RNAs, leading to their degradation or the inhibition of their translation [1, 4]. miR-205-5p is well-known for its dual role in human pathology, particularly in oncology, where it can act as either a tumor suppressor or an oncogene depending on the cellular context and the specific genes it targets [9, 20]. In many epithelial cancers, such as breast and prostate cancer, it is frequently downregulated and acts as a tumor suppressor by inhibiting the epithelial-to-mesenchymal transition (EMT) through the targeting of transcription factors like ZEB1 and ZEB2 [4, 8]. Conversely, in other contexts like lung or cervical cancer, it may be upregulated and promote tumor progression [5, 25]. Beyond cancer, miR-205-5p is involved in regulating angiogenesis, wound healing, hair follicle stem cell activity, and metabolic processes like insulin sensitivity [10, 17, 21]. Therapeutic development focuses on restoring its levels using miR-205 mimics in suppressive environments or using antagomirs to block its activity in oncogenic settings, though challenges remain regarding targeted delivery and potential off-target effects [13, 16].
Post-transcriptional gene silencing via RNA interference (RNAi), involving mRNA degradation or translational repression of target genes such as ZEB1, ZEB2, HER3, and VEGFA [1, 4, 9].
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