Int J Med Sci 2013; 10(6):676-682. doi:10.7150/ijms.5528 This issue Cite
Research Paper
1. Department of Neurology, the Affiliated Southeast Hospital of Xiamen University, Zhangzhou, 363000, China.
2. Department of Thoracic Surgery, the Affiliated Tangdu Hospital of Fourth Military Medical University, Xi'an, 710038, China.
3. Department of Orthopaedics, the Affiliated Southeast Hospital of Xiamen University, Orthopaedic Center of People's Liberation Army, Zhangzhou, 363000, China.
* These author contributed equally to this work.
Aberrant expression of MicroRNAs (miRNAs) has been implicated in several types of cancer. As a direct target gene of p53, miR-34a has been suggested to mediate the tumor suppressor function of p53. Ether à go-go 1 (Eag1) channel is overexpressed in a variety of cancers and plays important roles in cancer progression. However, the link between miR-34a and Eag1 in cancer is unclear. In this study, we used human osteosarcoma as the model to demonstrate that miR-34a was significantly downregulated in osteosarcoma tissues and cell lines compared with normal brain tissues and osteoblastic cell line. Next we evaluated the role of miR-34a in the regulation of osteosarcoma cell proliferation by CCK-8 and colony formation assays. The results showed that overexpression of miR-34a inhibited the proliferation of MG-63 and Saos-2 cells. Furthermore, xenograft nude mice model showed that miR-34a inhibited osteosarcoma growth in vivo. Mechanistically, we found that overexpression of miR-34a led to decreased Eag1 expression in osteosarcoma cells while inhibition of miR-34a increased Eag1 expression. Taken together, our results suggest that miR-34a could inhibit osteosarcoma growth via the down regulation of Eag1 expression.
Keywords: Ether à go-go1 (Eag1), MicroRNA-34a, proliferation, osteosarcoma, target gene.