MicroRNA-93 (miR-93) (miR-93)

MicroRNA-93 (miR-93) is a small non-coding RNA molecule that serves as a critical post-transcriptional regulator of gene expression [1, 4]. It is a member of the miR-106b-25 cluster and is located on human chromosome 7 [1, 6]. miR-93 functions by binding to the 3' untranslated regions (UTRs) of target mRNAs, leading to their degradation or the inhibition of their translation via the RNA-induced silencing complex (RISC) [4, 7]. This molecule plays a complex, dual role in human diseases, particularly in cancer, where it can act as either an oncogene or a tumor suppressor depending on the tissue context [1, 2, 3]. It is frequently overexpressed in lung, liver, and prostate cancers, promoting tumor growth and metastasis by targeting pathways such as PI3K/Akt and genes like PTEN [2, 4]. In addition to its role in oncology, miR-93 is implicated in the pathogenesis of diabetes, cardiovascular disorders, and chronic kidney disease [1, 6]. Therapeutic approaches targeting miR-93 involve the use of synthetic mimics to restore its levels or antagomirs to silence its activity [8, 11, 13]. However, the clinical development of these therapies faces significant challenges, including off-target effects and the need for efficient delivery systems to target tissues [12, 14, 16].

Other names

MIR93hsa-miR-93miR-93-5pmiR-93-3pMicroRNA 93miR-106b-25 cluster member

MicroRNA-93 regulates gene expression through the RNA interference (RNAi) pathway. It is incorporated into the RNA-induced silencing complex (RISC), where it guides the complex to complementary sequences in the 3' untranslated regions (UTRs) of target mRNAs [4, 7]. This interaction results in either the degradation of the mRNA transcript or the repression of its translation, thereby reducing the expression of the encoded protein [5, 7].