MicorRNA 106b ∼ 25 cluster and gastric cancer

Conventional strategies for the early diagnosis and treatment of gastric cancer are not yet satisfactory, and it calls for better diagnosis and treatments based on a deeper understanding of the molecular mechanisms. It has been revealed that the number of verified human microRNA (miRNA) expression contribute to the initiation and progression of cancer. Among them, miR-106b ∼ 25 cluster is of particular interest. The miRNA-106b ∼ 25 cluster is composed of the highly conserved miRNA-106b, miRNA-93 and miRNA-25. The miRNA-106b ∼ 25 polycistron exerted potential proliferative, anti-apoptotic and cell cycle-promoting effects on cancer cells. Over-expression of the miRNA-106b ∼ 25 cluster is known to overcome TGF-beta mediated growth suppression via targeting p21 and Bim. This cluster can additionally target the inhibitory Smad7 protein and increase TGF-beta RI which is sufficient to induce epithelial-to-mesenchymal transition (EMT). MiRNA-93 can promote angiogenesis. The tumor suppressor genes RB and PTEN are the direct targets of miRNA-106b ∼ 25. Especially, miRNA-106b ∼ 25 clusters play an important role in oncogenesis of gastric cancer. Focus on the essential role in tumorgenisis and extremely low expression of miRNA-106b ∼ 25 in normal tissues, it maybe an appropriate target of gastric cancer treatment and a novel biomarkers for detecting gastric cancer.