microRNA-200c (miR-200c)

microRNA-200c is a critical member of the miR-200 family of non-coding RNAs that plays a fundamental role in maintaining epithelial cell identity. Its primary biological function is the regulation of the epithelial-mesenchymal transition (EMT) by targeting the ZEB1 and ZEB2 transcription factors, which are known repressors of E-cadherin [Gregory et al., 2008, Nature Cell Biology]. In the context of oncology, miR-200c is frequently downregulated in various solid tumors, and its loss is strongly associated with increased metastatic potential, chemoresistance, and poor patient prognosis [Cochrane et al., 2009, Molecular Cancer Therapeutics]. Beyond cancer, miR-200c is involved in regulating oxidative stress responses and fibrotic pathways in cardiovascular and metabolic diseases [Magenta et al., 2011, Circulation Research]. Therapeutic interest in miR-200c focuses on the use of microRNA mimics to restore its expression in tumors, thereby reversing EMT and potentially sensitizing cancer cells to conventional chemotherapy. Conversely, antagomirs (antisense oligonucleotides) are explored in conditions where miR-200c overexpression may be pathological, such as in certain fibrotic or inflammatory states [Humphries and Yang, 2015, Cancer Letters]. Despite its therapeutic promise, clinical application is currently limited by the challenges of targeted delivery and the potential for off-target effects within complex gene networks. Research continues to evaluate miR-200c as a non-invasive liquid biopsy biomarker due to its stability in blood and correlation with disease progression [Juracek et al., 2019, Molecular Therapy - Nucleic Acids].

Other names

hsa-miR-200c-3phsa-miR-200c-5pMIR200CMicroRNA 200cmiR-200c-3p

MicroRNA-200c acts by binding to the 3'-untranslated region (3'-UTR) of target messenger RNAs (mRNAs), particularly those encoding the transcription factors ZEB1 and ZEB2. This binding leads to translational repression or mRNA degradation, which prevents the suppression of E-cadherin and maintains the epithelial phenotype of cells, thereby inhibiting the epithelial-mesenchymal transition (EMT) process [Park et al., 2008, Genes & Development].