miR-1 as a tumor suppressive microRNA targeting TAGLN2 in head and neck squamous cell carcinoma
Metrics: PDF 5067 views | HTML 5582 views | ?
1Department of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan
2Department of Otorhinolaryngology/Head and Neck Surgery, Chiba University Graduate School of Medicine, Chiba, Japan
3Department of Gynecologic Oncology, Chiba University Graduate School of Medicine, Chiba, Japan
4Department of Urology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan
*These authors contributed equally to this work.
Keywords: microRNA, miR-1, TAGLN2, tumor suppressor, HNSCC, microarray, oncogenes, oncotargets
Received: December 20, 2010; Accepted: January 23, 2011; Published: January 25, 2011;
Nijiro Nohata, e-mail:
Based on the microRNA (miRNA) expression signatures of hypopharyngeal and esophageal squamous cell carcinoma, we found that miR-1 was significantly down-regulated in cancer cells. In this study, we investigated the functional significance of miR-1 in head and neck squamous cell carcinoma (HNSCC) cells and identified miR-1-regulated novel cancer pathways. Gain-of-function studies using miR-1 revealed significant decreases in HNSCC cell proliferation, invasion, and migration. In addition, the promotion of cell apoptosis and cell cycle arrest was demonstrated following miR-1e transfection of cancer cells. A search for the targets of miR-1 revealed that transgelin 2 (TAGLN2) was directly regulated by miR-1. Silencing of TAGLN2 significantly inhibited cell proliferation and invasion in HNSCC cells. Down-regulation of miR-1 and up-regulation of TAGLN2 were confirmed in HNSCC clinical specimens. Our data indicate that TAGLN2 may have an oncogenic function and may be regulated by miR-1, a tumor suppressive miRNA in HNSCC. The identification of novel miR-1-regulated cancer pathways could provide new insights into potential molecular mechanisms of HNSCC carcinogenesis.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.