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MicroRNA 152 is a highly conserved, endogenous small non-coding RNA (microRNA) of the miR-148/152 family that negatively regulates gene expression by binding the 3' untranslated regions (3' UTRs) of specific mRNAs, leading to translational repression or mRNA degradation[1][2]. miR-152 plays crucial roles in the regulation of cell proliferation, apoptosis, immune modulation, and DNA methylation[1][2]. It is frequently downregulated in multiple cancers by promoter hypermethylation, resulting in derepression of oncogenic targets and contributing to tumorigenesis; restoration of its expression suppresses tumor cell growth, migration, and metastasis[1][2][4]. In cardiovascular disease, miR-152 has been shown to worsen cardiac function when overexpressed, while its pharmacological inhibition can protect against heart failure in preclinical models[3]. miR-152 is recognized both as a potential biomarker and a therapeutic target, but context-dependent duality in some cancers and technical challenges in RNA-based therapy development remain active areas of investigation[1][2][3][4][5].
miR-152 inhibition with antisense oligonucleotides leads to upregulation of its target genes and preservation of function in heart failure models[3]. Demethylating agents restore endogenous miR-152, reversing target silencing and tumor suppression[2].
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