CREPT regulated by miR-138 promotes breast cancer progression
Journal Article
·
· Biochemical and Biophysical Research Communications
- Department of General Surgery, Yantaishan Hospital, Yantai City, Shandong Province, 264000 (China)
- The 21 Ward of General Surgery, Daqing Oil Field General Hospital, Daqing, Heilongjiang, 163000 (China)
- Department of General Surgery, People's Hospital of Anqiu City, Anqiu City, Shandong Province, 262100 (China)
CREPT (also known as RPRD1B) function as an oncogene and is highly expressed in several kinds of cancers. However, the distribution and clinical significance of CREPT in breast cancer (BC) still not clarified. In this study, we found that the CREPT expression is greatly upregulated in BC tissues and cell lines. Moreover, the CREPT expression was significantly associated with tumor differentiation and metastasis. Next, the functional assay of CREPT showed that CREPT could promote BC proliferation and invasion both in vitro and in vivo. Dual-luciferase reporter assay indicated that miR-138 regulated the expression of CREPT by binding to its 3′-UTR. miR-138 is downregulated and inversely correlated with CREPT expression in BCs. Overexpression of miR-138 suppressed tumor growth and invasion, these effects could be reversed by re-expressing CREPT. Mechanistically, CREPT regulated β-catenin/TCF4/cyclin D1 pathway in BC. In conclusion, the data suggested that miR-138/CREPT involved BC progression, providing potential therapeutic targets for BC. - Highlights: • CREPT expression is greatly upregulated in BC tissues and cell lines. • CREPT could promote BC proliferation and invasion both in vitro and tumor growth in vivo. • CREPT is a direct target of miR-138 in breast cancer. • MiR-138 suppressed BC progression by repressing CREPT. • CREPT regulates β-catenin/TCF4/cyclin D1 pathway in BC.
- OSTI ID:
- 22719123
- Journal Information:
- Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 1 Vol. 493; ISSN 0006-291X; ISSN BBRCA9
- Country of Publication:
- United States
- Language:
- English
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