The epithelial-mesenchymal transition (EMT) is a process driving invasion, recurrence, and metastasis of gastric cancer, and EMT is triggered by specific physiological factors that arise during tumorigenesis, such as hypoxia. Identifying the molecular mechanisms underlying EMT will potentially yield insight into the pathways fueling cancer recurrence and metastasis and thus, lead to novel molecular targets that will improve treatment of the disease. The microRNA210 (MIR210) is such a candidate molecule mediating EMT in gastric cancer based on a number of observations. First, MIR210 is often highly overexpressed in gastric cancer. Second, MIR210 is a hypoxia-specific miRNA, and its expression is significantly increased in hypoxic environments where EMT develops. Third, MIR210 is regulated by hypoxia inducible factor 1α (HIF-1α), a key transcription factor mediating important tumor associated processes such as EMT and angiogenesis in response to hypoxia during tumorigenesis. Finally, MIR210 has been intriguingly associated with Helicobacterpylori infection, which typically develops in an anaerobic environment and is known to have a causal role in the development of gastric cancer. Although studies have shown that MIR210 is often highly expressed in gastric cancer and associated with specific pathological conditions, functional experiments have not yet been performed to determine the role of MIR210 and downstream mediators in the development and progression of gastric cancer. Here, MIR210 is proposed as a viable molecular target in the treatment of gastric cancer, specifically for the inhibition of invasion and metastasis.
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