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Updated: Feb 23, 2026

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
Published on: February 21, 2014
CREPT regulated by miR-138 promotes breast cancer progression
Zhi Liang1, Qi Feng2, Licheng Xu1
1Department of General Surgery, Yantaishan Hospital, Yantai City, Shandong Province, 264000, PR China.
Abstract:
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.
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