| Literature DB >> 26101708 |
Wenjuan Wu1, Xizhi Zhang2, Yuexia Liao3, Weicheng Zhang3, Haichao Cheng3, Zijing Deng3, Jingyuan Shen3, Qing Yuan3, Yu Zhang3, Weigan Shen4.
Abstract
miR-30c has been reported to act as a tumor suppressor and negatively regulate cancer metastasis by directly targeting metastasis associated genes; however, miR-30c has also been shown to promote the invasion of metastatic breast cancer cells, suggesting that miR-30c might be involved in cancer cell metastasis in different ways via targeting different genes. In this study, we demonstrated that over-expression and knockdown of immediate early response protein 2 (IER2) modulated the general capacity of the migration and invasion in hepatocellular carcinoma cell line SMMC-7721 and HepG2, whereas overexpression and knockdown of miR-30c decreased and promoted cell motility, respectively. Further studies revealed that miR-30c overexpression down-regulated the expression of IER2 protein but not its mRNA level, and miR-30c can directly target the 3' untranslated region (3'UTR) of IER2, and subsequently reducing its expression. Moreover, we also showed that suppression of cell motility by miR-30c was partially rescued by IER2 re-expression. Our results indicated that miR-30c may function as a negative regulator in cell motility, with IER2 as a direct and functional target in SMMC-7721 and HepG2 cells.Entities:
Keywords: IER2; invasion; miR-30c; migration
Year: 2015 PMID: 26101708 PMCID: PMC4473321
Source DB: PubMed Journal: Am J Cancer Res ISSN: 2156-6976 Impact factor: 6.166