CREPT regulated by miR-138 promotes breast cancer progression

Biochem Biophys Res Commun. 2017 Nov 4;493(1):263-269. doi: 10.1016/j.bbrc.2017.09.033. Epub 2017 Sep 8.

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.

Keywords: Breast cancer; CREPT; Invasion; MiR-138; Proliferation.

MeSH terms

  • Animals
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology*
  • Cell Cycle Proteins / metabolism*
  • Cell Proliferation
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • MCF-7 Cells
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • MicroRNAs / metabolism*
  • Neoplasm Invasiveness
  • Neoplasm Proteins / metabolism*
  • Tumor Cells, Cultured

Substances

  • Cell Cycle Proteins
  • MIRN138 microRNA, human
  • MicroRNAs
  • Neoplasm Proteins
  • RPRD1B protein, human