Literature DB >> 29970662

Post-transcriptional regulation DPC4 gene by miR-190 in colorectal cancer cells.

Bin Xie1, Zhenghao Deng1, Yu Pan1, Chunyan Fu1, Songqing Fan2, Yongguang Tao3, Jianhua Zhou1, Desheng Xiao1.   

Abstract

OBJECTIVE: The objective of this study is to elucidate the regulation of the DPC4 gene by miR-190 in colorectal cancer (CRC) cells. The present study was undertaken to determine whether the DPC4 gene is a target gene of miRNA-190, identify target motifs and to elucidate the mechanism of regulation of DPC4 by miRNA-190.
MATERIALS AND METHODS: MiR-190 and DPC4 expression were measured in five different CRC cell lines by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. The regulation of DPC4 by miR-190 was evaluated by qRT-PCR, Western blotting, and luciferase reporter assays in the human CRC cell line HT-29 after treatment with miR-190 mimics and inhibitors.
RESULTS: The DPC4 mRNA, miR-, and DPC4 protein expression levels were highest in LS174T cells while lowest in SW480 and SW620 cells. The DPC4/miR-190 ratio in the HT-29 cancer cell line was the largest. MiR-190 expression increased dramatically after treatment with miR-190 mimics and decreased significantly after treatment with miR-190 inhibitors. DPC4 protein expression decreased in the miR-190 mimics transfection group when compared to the negative control (N.C.) group and increased in the miR-190 inhibitor groups when compared to the inhibitor plus N.C. group. MiR-190 inhibits the relative luciferase activity of psiCHECK-2™ vector-3'UTR compared to the N.C. group, while miR-190 had no obvious effect on the relative luciferase activity of the psiCHECK-2™ vector-3'UTRmut and psiCHECK-2™ vector transfected cells.
CONCLUSIONS: The DPC4 gene might be the target gene of miR-190, which may negatively regulate the DPC4 gene in human CRC cells by translational suppression rather than mRNA degradation.

Entities:  

Keywords:  Colorectal cancer; DPC4 gene; miR-190; posttranscriptional regulation

Mesh:

Substances:

Year:  2018        PMID: 29970662     DOI: 10.4103/jcrt.JCRT_577_17

Source DB:  PubMed          Journal:  J Cancer Res Ther        ISSN: 1998-4138            Impact factor:   1.805


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