CTNNA3 is a tumor suppressor in hepatocellular carcinomas and is inhibited by miR-425
Metrics: PDF 631 views | HTML 799 views | ?
Bing He1,*, Ting Li1,*, Lei Guan1,*, Fang-E Liu2, Xue-Mei Chen1, Jing Zhao1, Song Lin1, Zhi-Zhen Liu1, Hu-Qin Zhang1
1The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, P.R. China
2The Center of Basic Medicine Teaching Experiments, School of Basic Medicine, Fourth Military Medicine University (FMMU), Xi’an 710032, P.R. China
*These authors contributed equally to this work
Hu-Qin Zhang, e-mail: email@example.com
Keywords: CTNNA3, miR-425, HCC, proliferation, invasion
Received: July 02, 2015 Accepted: January 07, 2016 Published: January 22, 2016
Hepatocellular carcinoma (HCC) is a common and leading cause of death worldwide. Here, we identified that a cell-cell adhesion gene, CTNNA3, is a tumor suppressor in HCC. CTNNA3 inhibited the proliferation, migration and invasion of HCC cell lines. In these cells, CTNNA3 inhibited Akt signal, and in turn decreased the proliferating cell nuclear antigen (PCNA) and the matrix metallopeptidase MMP-9, and increased the cell cycle inhibitor p21Cip1/Waf1. Meanwhile, CTNNA3 is inhibited by miR-425 in HCC. The miR-425 directly bound to the 3′UTR of CTNNA3 and inhibited its expression. The tumor suppressor function of CTNNA3 and the oncogenic function of miR-425 were further confirmed in HCC cell xenograft in nude mice. The miR-425/CTNNA3 axis may provide insights into the mechanisms underlying HCC, and contribute to potential therapeutic strategy of HCC.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.