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Title: CREPT regulated by miR-138 promotes breast cancer progression

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. - 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/cyclinmore » D1 pathway in BC.« less

Authors:
 [1];  [2];  [1];  [1];  [3]
  1. Department of General Surgery, Yantaishan Hospital, Yantai City, Shandong Province, 264000 (China)
  2. The 21 Ward of General Surgery, Daqing Oil Field General Hospital, Daqing, Heilongjiang, 163000 (China)
  3. Department of General Surgery, People's Hospital of Anqiu City, Anqiu City, Shandong Province, 262100 (China)
Publication Date:
OSTI Identifier:
22719123
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 493; Journal Issue: 1; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANIMAL TISSUES; IN VITRO; IN VIVO; LUCIFERASE; MAMMARY GLANDS; METASTASES; NEOPLASMS; ONCOGENES

Citation Formats

Liang, Zhi, Feng, Qi, Xu, Licheng, Li, Shuyan, and Zhou, Lei. CREPT regulated by miR-138 promotes breast cancer progression. United States: N. p., 2017. Web. doi:10.1016/J.BBRC.2017.09.033.
Liang, Zhi, Feng, Qi, Xu, Licheng, Li, Shuyan, & Zhou, Lei. CREPT regulated by miR-138 promotes breast cancer progression. United States. doi:10.1016/J.BBRC.2017.09.033.
Liang, Zhi, Feng, Qi, Xu, Licheng, Li, Shuyan, and Zhou, Lei. Sat . "CREPT regulated by miR-138 promotes breast cancer progression". United States. doi:10.1016/J.BBRC.2017.09.033.
@article{osti_22719123,
title = {CREPT regulated by miR-138 promotes breast cancer progression},
author = {Liang, Zhi and Feng, Qi and Xu, Licheng and Li, Shuyan and Zhou, Lei},
abstractNote = {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.},
doi = {10.1016/J.BBRC.2017.09.033},
journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 1,
volume = 493,
place = {United States},
year = {2017},
month = {11}
}