MicroRNA-542-3p suppresses cell growth of gastric cancer cells via targeting oncogene astrocyte-elevated gene-1
Xinsheng Shena b, Yaqing Sia b, Zhugong Yangc d, Qun Wanga b, Jiaxiang Yuana b, Xiefu Zhangb e✉
- aDepartment of Minimally Invasive Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China
- bThe First Affiliated Hospital of Zhengzhou University
- cDepartment of Blood Collection, Henan Red Cross Blood Center, Zhengzhou, 450053, Henan, China
- dHenan Red Cross Blood Center
- eDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, No. 1 East Jianshe Road, Zhengzhou, 450052, Henan, China
- ✉Corresponding author
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Abstract
MicroRNAs (miRNAs) have been suggested to play critical roles in tumorigenesis as well as in the development of therapies for the treatment of cancers. However, the tumor-associated miRNAs in gastric cancers remain poorly understood. Here, we report on miR-542-3p in gastric cancers, which has been widely studied in other cancers as a tumor suppressor. Real-time quantitative PCR analysis demonstrated that miR-542-3p was significantly down-regulated in gastric cancer tissues (p < 0.0001) and cell lines (p < 0.001). Overexpression of miR-542-3p significantly inhibited cell growth of gastric cancer cells both in vitro (p < 0.01) and in vivo (p < 0.01). Notably, overexpression of miR-542-3p apparently reduced the protein expression of astrocyte-elevated gene-1 (AEG-1) (p < 0.01). The dual-luciferase reporter assay validated that miR-542-3p directly bound the 3'-untranslated region (UTR) of AEG-1, which could be abolished by mutation of the predicted miR-542-3p binding site. Furthermore, overexpression of miR-542-3p markedly inhibited the activation of oncogenic signaling pathways including the Akt, β-catenin and nuclear factor-κB pathways. Additionally, overexpression of AEG-1 without the 3'-UTR partially reversed the cell growth arrest induced by miR-542-3p overexpression in gastric cancer cells (p < 0.05). Taken together, these data suggest that miR-542-3p might function as a tumor suppressor in gastric cancer, potentially by targeting the oncogene AEG-1, implying a potential role for miR-542-3p in the development of therapeutic methods for gastric cancer.
TL;DROverexpression of miR-542-3p markedly inhibited the activation of oncogenic signaling pathways including the Akt, β-catenin and nuclear factor-κB pathways and suggested a potential role in the development of therapeutic methods for gastric cancer. (Semantic Scholar)