Hepatocyte growth factor receptor messenger RNA (MET mRNA) (MET mRNA)

c-MET mRNA is the messenger RNA transcript of the MET proto-oncogene, which encodes the Hepatocyte Growth Factor Receptor (HGFR), a transmembrane receptor tyrosine kinase [1, 2]. This mRNA serves as the essential template for the synthesis of the c-MET protein, which plays a critical role in cell proliferation, survival, and epithelial-mesenchymal transition (EMT) through the activation of downstream signaling pathways like PI3K/AKT and MAPK [2, 5]. In various cancers, such as non-small cell lung cancer (NSCLC) and gastric cancer, the c-MET mRNA is often dysregulated via overexpression or oncogenic splicing variants, most notably the MET exon 14 skipping mutation which leads to decreased protein degradation and prolonged signaling [5]. Therapeutic strategies targeting c-MET mRNA, including small interfering RNAs (siRNAs) like TKM-080301 and microRNA mimics like MRX34, aim to degrade the transcript or modulate its translation to prevent the production of the oncogenic protein [3, 4]. While small molecule inhibitors and monoclonal antibodies targeting the c-MET protein are more clinically established, RNA-targeted approaches offer a distinct mechanism to silence the MET pathway at the pre-translational level [3, 5].

Other names

c-MET mRNAMET mRNAHepatocyte growth factor receptor mRNAMET proto-oncogene, receptor tyrosine kinase mRNAHGFR mRNA

The primary mechanisms of action for drugs targeting c-MET mRNA include RNA interference (siRNA), where small double-stranded RNAs guide the cleavage of the target mRNA by the RISC complex, and antisense-mediated degradation, where single-stranded oligonucleotides induce RNase H-mediated cleavage of the mRNA-DNA heteroduplex. Additionally, microRNA mimics can bind to the 3' untranslated region (UTR) of the mRNA to repress translation or promote degradation.