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MicroRNA 10b-5p-regulated messenger RNAs (mRNAs) represent a diverse network of transcripts whose expression is post-transcriptionally controlled by the microRNA miR-10b-5p. This microRNA is a well-characterized oncomiR that is frequently overexpressed in metastatic cancers, such as breast cancer and glioblastoma, where it suppresses key tumor-suppressive mRNAs like HOXD10, PTEN, and KLF4 to promote cell invasion and the epithelial-mesenchymal transition (EMT) [1, 3, 5]. In other pathological contexts, such as diabetes and neurodegeneration, miR-10b-5p levels may be depleted, leading to the dysregulation of targets like KLF11 and BDNF, which affects glucose homeostasis and neuronal survival [10, 11]. Therapeutic strategies primarily involve the use of antisense oligonucleotides (antagomirs), such as TTX-MC138, to inhibit miR-10b-5p and restore the expression of its suppressed mRNA targets in oncology [3, 9]. Alternatively, miRNA mimics are being explored to replenish its regulatory function in metabolic diseases where the miRNA is downregulated [11]. Clinical and preclinical efforts focus on optimizing delivery systems, such as lipid or magnetic nanoparticles, to overcome biological barriers like the blood-brain barrier and minimize off-target effects associated with the broad regulatory network of this miRNA [5, 9].
Antisense inhibition of miR-10b-5p to prevent the degradation or translational repression of target mRNAs (antagomirs); or use of miRNA mimics to enhance the suppression of specific target mRNAs.
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