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MicroRNA-363 is a short (20–24 nucleotide) non-coding RNA molecule that belongs to the microRNA family[2]. It regulates gene expression by binding to the 3' untranslated regions of target messenger RNAs (mRNAs), typically leading to translational inhibition or target mRNA degradation[2]. miR-363 plays a critical role in controlling cell proliferation, cell cycle progression, apoptosis, migration, and invasion, particularly in the context of cancer biology[1][3]. Dysregulation of miR-363 expression has been implicated in a spectrum of diseases, predominantly malignancies but also neurodegenerative and cardiovascular diseases[1][2][3][4]. In cancer, miR-363 often acts as a tumor suppressor: its overexpression can inhibit tumor progression by negatively regulating oncogenic targets such as E2F3, PCNA, Sox4, SphK2, and HMGA2, and by modulating key signaling pathways, including mTOR and ERK[1][3]. Low expression of miR-363 is associated with poor prognosis and increased metastatic potential in several tumor types[1]. While experimental modulation of miR-363 (using mimics or inhibitors) is being explored as a therapeutic approach, no direct drugs targeting miR-363 have reached clinical practice[1][2][3].
miRNA mimics/inhibitors modulate gene expression post-transcriptionally by either inhibiting or increasing miR-363 activity, thereby altering the expression of its target mRNAs (such as E2F3, PCNA, Sox4, HMGA2)[1][3].
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