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Mol Carcinog. 2018 Oct;57(10):1408-1420. doi: 10.1002/mc.22866. Epub 2018 Jul 3.

MicroRNA-383 acts as a tumor suppressor in colorectal cancer by modulating CREPT/RPRD1B expression.

Author information

1
School of Environmental and Chemical Engineering, Yanshan University, Qinhuangdao, Hebei Province, China.
2
Department of Molecular Biosciences, University of Kansas, Lawrence, Kansas.
3
Institute of Immunology, Medical School, Third Military Medical University, Chongqing, China.
4
State Key Laboratory of Membrane Biology, School of Medicine, National Engineering Laboratory for anti-tumor Therapeutics, Tsinghua University, Beijing, China.
5
Department of Psychological Sciences, Purdue University, West Lafayette, Indiana.
6
Department of General Surgery and Pathology, Chinese PLA General Hospital, Beijing, China.

Abstract

CREPT (Cell-cycle-related and expression-elevated protein in tumor)/RPRD1B, a novel protein that enhances the transcription of Cyclin D1 to promote cell proliferation during tumorigenesis, was demonstrated highly expressed in most of tumors. However, it remains unclear how CREPT is regulated in colorectal cancers. In this study, we report that miR-383 negatively regulates CREPT expression. We observed that CREPT was up-regulated but the expression of miR-383 was down regulated in both colon cancer cell lines and colon tumor tissues. Intriguingly, we found that enforced expression of miR-383 inhibited the expression of CREPT at both the mRNA and protein level. Using a luciferase reporter, we showed that miR-383 targeted the 3'-UTR of CREPT mRNA directly. Consistently we observed that over expression of miR-383 shortened the half-life of CREPT mRNA in varieties of colorectal cancer cells. Furthermore, restoration of miR-383 inhibited cell growth and colony formation of colon cancer cells accompanied by inhibition of expression of CREPT and related downstream genes. Finally, we demonstrated that stable over expression of miR-383 in colon cancer cells decreased the growth of the tumors. Our results revealed that the abundant expression of CREPT in colorectal cancers is attributed to the decreased level of miR-383. This study shed a new light on the potential therapeutic therapy strategy for colorectal cancers using introduced miRNA.

KEYWORDS:

CREPT; colony formation; colorectal cancer; miR-383; tumor growth

PMID:
29938829
PMCID:
PMC6324535
[Available on 2019-10-01]
DOI:
10.1002/mc.22866
[Indexed for MEDLINE]

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