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microRNA-144 (miR-144) is a small, non-coding RNA molecule located on the long arm of chromosome 17 (17q11.2) in humans that functions as a post-transcriptional regulator of gene expression[3][5]. Through base pairing with target mRNAs, miR-144 directs genes for silencing by either translation inhibition or mRNA degradation. It plays crucial roles in diverse biological processes, including regulating cell proliferation, apoptosis, inflammation, energy metabolism, and epithelial-mesenchymal transition (EMT)[1][2][3]. miR-144 is generally recognized as a tumor suppressor, inhibiting oncogenic pathways in multiple cancers, though in some cancers it may have context-specific pro-tumorigenic effects[3][4]. Its dysregulation is implicated in cancer progression, inflammatory diseases, and potential neuropsychiatric disorders. Due to its involvement in disease-relevant signaling pathways (e.g., PI3K/Akt, EGFR/Src/AKT, NF-κB), miR-144 is actively studied as a biomarker and as a candidate for RNA-targeted therapies. However, the complexity of its regulatory network presents clinical translation challenges related to specificity and safety[2][3][4].
Antagomirs: inhibit endogenous miR-144, upregulating target genes; Mimics: restore or enhance miR-144 activity, suppressing target mRNAs; Post-transcriptional silencing of specific mRNAs, e.g., those encoding EMT factors (ZEB1/2), kinases (ROCK1, MAP3K8), and transcription factors (HOXA10, Notch-1, HIF-1α, Nrf2, EGFR)[1][2][3].
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