MicroRNA 34a (hsa-miR-34a) (miR-34a)

Mature hsa-miR-34a is a highly conserved, 22-nucleotide non-coding RNA that functions as a potent tumor suppressor and a key mediator of the p53-regulated stress response [NIH, 2025; MDPI, 2021]. It post-transcriptionally silences a broad network of over 30 oncogenes, including MYC, MET, BCL2, and CDK4/6, thereby inducing apoptosis, G1 cell cycle arrest, and senescence while inhibiting the epithelial-mesenchymal transition (EMT) and cancer stemness [NIH, 2020; Frontiers, 2021]. In many malignancies, miR-34a is frequently downregulated or epigenetically silenced, which has led to the development of miRNA replacement therapies such as MRX34, a liposomal miR-34a mimic [NIH, 2020; MDPI, 2021]. Although early clinical trials demonstrated proof-of-concept for target modulation, they were halted due to severe immune-mediated adverse events and cytokine release syndrome [BioWorld, 2016; NIH, 2020]. Beyond its role in oncology, miR-34a is implicated in the pathogenesis of cardiovascular and neurodegenerative diseases, where it can promote pathological apoptosis and senescence, making it a target for both mimicry and inhibition depending on the disease context [Frontiers, 2022; NIH, 2022].

Other names

hsa-miR-34a-5pMIR34AMIRN34AMicroRNA 34a-5pMature miR-34a

Mature hsa-miR-34a acts through the RNA-induced silencing complex (RISC) to post-transcriptionally repress target mRNAs by binding to their 3'-untranslated regions (3'-UTRs) [miRBase; NIH, 2025]. This leads to mRNA degradation or translational inhibition of key oncogenic and pro-survival factors such as MYC, MET, BCL2, and CDK4/6 [NIH, 2020; NIH, 2025]. In therapeutic contexts, miR-34a mimics restore this tumor-suppressive function in deficient cells, while anti-miR oligonucleotides are used to inhibit its pro-apoptotic effects in conditions like cardiovascular disease [NIH, 2019; Frontiers, 2022].