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Surg Oncol. 2013 Jun;22(2):e7-10. doi: 10.1016/j.suronc.2013.01.003. Epub 2013 Mar 17.

MicorRNA 106b ∼ 25 cluster and gastric cancer.

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  • 1Cancer Prevention Center, Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Cancer Prevention and Therapy, Huanhuxi Road, Hexi District, Tianjin 300060, China.

Abstract

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.

Copyright © 2013 Elsevier Ltd. All rights reserved.

PMID:
23510949
[PubMed - indexed for MEDLINE]
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