MicroRNA-146a promote cell migration and invasion in human colorectal cancer via carboxypeptidase M/src-FAK pathway
Metrics: PDF 1784 views | HTML 1837 views | ?
Di Lu1,*, Qunyan Yao1,*, Cheng Zhan2, Zhang Le-Meng3, Hongchun Liu1, Yu Cai1, Chuantao Tu1, Xi Li1, Yanting Zou1, Shuncai Zhang1
1Department of Gastroenterology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China
2Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China
3Department of The Affiliated Cancer Hospital, Xiang Ya School of Medicine, Central South University, Changsha, Hunan, 410013, China
*These authors contributed equally to this work
Keywords: miR-146a-5p, carboxypeptidase M, colorectal cancer, migration, invasion
Received: May 07, 2016 Accepted: January 23, 2017 Published: February 07, 2017
Colorectal cancer (CRC) is one of the most common cancers worldwide, and microRNAs play important roles in CRC progression. This study aimed to investigate the roles of miR-146a-5p in human CRC and their molecular mechanisms. First, we found that miR-146a-5p was significantly upregulated in CRC tissues and promoted the migration of CRC cells. Then, we identified carboxypeptidase M (CPM) as a direct target of miR-146a-5p, and found that it inhibited the migration and invasion of CRC cells. Our results also showed that CPM expression was positively correlated with overall survival and negatively correlated with recurrence, lymph node invasion, and N stage. Furthermore, we demonstrated that both miR-146a-5p and CPM regulated Src and FAK expression, while the Src-FAK signaling pathway is widely known to be associated with the migration and invasion of multiple tumor cells. This study is the first to demonstrate the functional and mechanistic relationship of the miR-146a-5p/CPM/Src-FAK axis and its effect on the migration and invasion of CRC cells. Thus, miR-146a-5p represents potential targets for CRC diagnosis and therapy.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.