The interplay of signaling pathways and miRNAs in the pathogenesis and targeted therapy of esophageal cancer

Globally, esophageal cancer (EC) is the 6th leading cause of cancer-related deaths and the second deadliest gastrointestinal cancer. Multiple genetic and epigenetic factors, such as microRNAs (miRNAs), influence its onset and progression. miRNAs are short nucleic acid molecules that can regulate multiple cellular processes by regulating gene expression. Therefore, EC initiation, progression, apoptosis evasions, invasion capacity, promotion, angiogenesis, and epithelial-mesenchymal transition (EMT) enhancement are associated with miRNA expression dysregulation. Wnt/-catenin signaling, Mammalian target of rapamycin (mTOR)/P-gp, phosphoinositide-3-kinase (PI3K)/AKT/c-Myc, epidermal growth factor receptor (EGFR), and transforming growth factor (TGF)-& beta; signaling are crucial pathways in EC that are controlled by miRNAs. This review was conducted to provide an up-to-date assessment of the role of microRNAs in EC pathogenesis and their modulatory effects on responses to various EC treatment modalities.

Automated summary

Esophageal cancer is a major cause of cancer-related deaths worldwide, and miRNAs play a crucial role in its pathogenesis and response to treatment. Dysregulation of miRNA expression is associated with various aspects of esophageal cancer, including initiation, progression, evasion of apoptosis, invasion, and epithelial-mesenchymal transition. Key pathways in esophageal cancer, such as Wnt/-catenin signaling, mTOR/P-gp, PI3K/AKT/c-Myc, EGFR, and TGF-β signaling, are modulated by miRNAs. This review provides an updated assessment of the role of miRNAs in esophageal cancer and their potential as therapeutic targets.