microRNA 4454 (MIR4454)

microRNA 4454 is a human microRNA that acts as a post-transcriptional regulator of gene expression by binding target mRNAs for degradation or translational inhibition[6]. It is derived from HERV-H (a human endogenous retroviral element), and its abnormal expression is documented in various cancers, such as bladder, colorectal, hepatic, ovarian, cervical, and lung adenocarcinoma, where it may regulate tumor suppressor genes (e.g., *DNAJB4*, *SASH1*, *GNL3L*) and influence cell proliferation, migration, apoptosis, inflammation, and resistance to chemotherapy[2][3][5][1]. In asthma and allergic rhinitis, it modulates epithelial cell function and inflammatory cytokine production via the NF-κB pathway[1]. Elevated or decreased levels of miR-4454 can thus serve as specific biomarkers for disease diagnosis and prognosis, and miR-4454 itself is being explored as a therapeutic target, primarily using synthetic mimics or inhibitors to restore or inhibit its function, respectively[2][3][5][1].

Other names

hsa-mir-4454MIR4454miR-4454

MIR4454 primarily acts by binding to mRNA 3'UTRs, leading to the suppression of target gene expression, which can include oncogenic or tumor suppressor genes (e.g., *GNL3L*, *DNAJB4*, *SASH1*). It also modulates *NF-κB* signaling pathways, thereby affecting inflammation and apoptosis, and regulates cytokine production (e.g., IL-17, IL-6, IL-8). Depending on the cellular context, these actions result in the inhibition of cell migration, proliferation, or the promotion of apoptosis.