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MicroRNA 543 (miR-543) is a small, non-coding RNA molecule that regulates gene expression post-transcriptionally, primarily by binding to the 3'-untranslated region (UTR) of specific mRNAs, leading to their degradation or translational inhibition[2][6][11]. It is transcribed from the MIR543 gene, which is located within the imprinted DLK1-DIO3 region on human chromosome 14[2][6][10][11]. miR-543 plays complex, context-dependent roles in human biology, acting either as an oncogene or tumor suppressor depending on the tissue and molecular environment: In pancreatic, gastric, renal, and oral squamous cell carcinomas, as well as some other cancers, miR-543 typically promotes cell proliferation, invasion, migration, and epithelial–mesenchymal transition, thus facilitating tumor progression.[1][3][4][7][9][12] In contrast, in some contexts such as colorectal cancer and glioblastoma, miR-543 can act as a tumor suppressor, inhibiting proliferation and metastasis by targeting genes like KRAS, MTA1, HMGA2, and ADAM9[5][8][10]. miR-543 is implicated in a broad range of systemic and organ-specific diseases, functioning as part of a complex non-coding RNA network affecting cell fate, EMT, apoptosis, and more[2][6]. miR-543's diversity of direct mRNA targets and variable regulatory effect make it a promising but complex potential biomarker and therapeutic target in oncology and other diseases[2][5][6]. However, as with many miRNAs, translation into clinical applications remains limited by delivery challenges, potential pleiotropic effects, and incomplete understanding of its broader role in normal physiology and disease[2][6].
Inhibition or restoration of miR-543 expression to modulate gene expression of its targets (e.g., targeting oncogenic or tumor suppressor pathways). It targets specific mRNAs such as SPOP, ADAM9, KRAS, MTA1, HMGA2, FAK, TWIST1, PTEN, PAQR3, SIRT1, PRMT9, CYP3A5, and DKK1, resulting in respective downstream effects in cell functions, proliferation, migration, and apoptosis
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