microRNA-143 (miR-143)

microRNA-143 (miR-143) is a small non-coding RNA molecule that plays a critical role in the post-transcriptional regulation of gene expression by binding to the 3-untranslated regions (UTRs) of target mRNAs. It is widely recognized as a potent tumor suppressor, and its expression is frequently downregulated in a variety of cancers, including colorectal, lung, and breast cancers. This downregulation leads to the overexpression of key oncogenic drivers such as KRAS, IGF1R, and BCL2, which promote cell proliferation, survival, and metastasis. Beyond oncology, miR-143 is essential for maintaining the contractile phenotype of vascular smooth muscle cells, and its dysregulation is linked to cardiovascular conditions like atherosclerosis and hypertension. Therapeutic approaches targeting miR-143 primarily involve the use of synthetic mimics or agomirs to restore its suppressive function, thereby inhibiting tumor progression and enhancing the efficacy of conventional chemotherapeutic agents like paclitaxel and 5-fluorouracil. However, the clinical translation of miR-143-based therapies faces significant challenges, including the need for stable delivery systems and the minimization of off-target effects. Additionally, miR-143 levels in tissue and serum are being investigated as potential diagnostic and prognostic biomarkers for cancer and cardiovascular risk. The miR-143/145 cluster is particularly important in vascular biology, where it regulates smooth muscle cell fate and plasticity. Overall, miR-143 represents a promising therapeutic target and biomarker across multiple disease areas, though delivery remains a primary hurdle.

Other names

miR-143hsa-miR-143MIR143microRNA 143

miR-143 mimics or agomirs function by binding to the 3-untranslated region (UTR) of target oncogenic mRNAs, such as KRAS and IGF1R, to induce mRNA degradation or translational repression, thereby restoring tumor-suppressive signaling and sensitizing cells to chemotherapy.