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Upregulated microRNA-92b regulates the differentiation and proliferation of EpCAM-positive fetal liver cells by targeting C/EBPß

microRNAs (miRNAs) are short noncoding RNAs that negatively regulate gene expression. Although recent evidences have been indicated that their aberrant expression may play an important role in cancer stem cells, the mechanism of their deregulation in neoplastic transformation of liver cancer stem ce...

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Published in:PloS one 2013-08, Vol.8 (8), p.e68004
Main Authors: Qian, Nian-Song, Liu, Wei-Hui, Lv, Wen-Ping, Xiang, Xin, Su, Ming, Raut, Vikram, Chen, Yong-Liang, Dong, Jia-Hong
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cited_by cdi_FETCH-LOGICAL-c5744-bf81eb69883104e202e5654e196ffd5a2cc2fad6c72c214c80a5ff9ab48855bf3
cites cdi_FETCH-LOGICAL-c5744-bf81eb69883104e202e5654e196ffd5a2cc2fad6c72c214c80a5ff9ab48855bf3
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container_issue 8
container_start_page e68004
container_title PloS one
container_volume 8
creator Qian, Nian-Song
Liu, Wei-Hui
Lv, Wen-Ping
Xiang, Xin
Su, Ming
Raut, Vikram
Chen, Yong-Liang
Dong, Jia-Hong
description microRNAs (miRNAs) are short noncoding RNAs that negatively regulate gene expression. Although recent evidences have been indicated that their aberrant expression may play an important role in cancer stem cells, the mechanism of their deregulation in neoplastic transformation of liver cancer stem cells (LCSCs) has not been explored. In our study, the HCC model was established in F344 rats by DEN induction. The EpCAM(+) cells were sorted out from unfractionated fetal liver cells and liver cancer cells using the FACS analysis and miRNA expression profiles of two groups were screened through microarray platform. Gain-of-function studies were performed in vitro and in vivo to determine the role of miR-92b on proliferation and differentiation of the hepatic progenitors. In addition, luciferase reporter system and gene function analysis were used to predict miR-92b target. we found that miR-92b was highly downregulated in EpCAM(+) fetal liver cells in expression profiling studies. RT-PCR analysis demonstrated reverse correlation between miR-92b expression and differentiation degree in human HCC samples. Overexpression of miR-92b in EpCAM(+) fetal liver cells significantly increased proliferation and inhibited differentiation as well as in vitro and in vivo studies. Moreover, we verified that C/EBPß is a direct target of miR-92b and contributes to its effects on proliferation and differentiation. We conclude that aberrant expression of miR-92b can result in proliferation increase and differentiation arrest of hepatic progenitors by targeting C/EBPß.
doi_str_mv 10.1371/journal.pone.0068004
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Although recent evidences have been indicated that their aberrant expression may play an important role in cancer stem cells, the mechanism of their deregulation in neoplastic transformation of liver cancer stem cells (LCSCs) has not been explored. In our study, the HCC model was established in F344 rats by DEN induction. The EpCAM(+) cells were sorted out from unfractionated fetal liver cells and liver cancer cells using the FACS analysis and miRNA expression profiles of two groups were screened through microarray platform. Gain-of-function studies were performed in vitro and in vivo to determine the role of miR-92b on proliferation and differentiation of the hepatic progenitors. In addition, luciferase reporter system and gene function analysis were used to predict miR-92b target. we found that miR-92b was highly downregulated in EpCAM(+) fetal liver cells in expression profiling studies. RT-PCR analysis demonstrated reverse correlation between miR-92b expression and differentiation degree in human HCC samples. Overexpression of miR-92b in EpCAM(+) fetal liver cells significantly increased proliferation and inhibited differentiation as well as in vitro and in vivo studies. Moreover, we verified that C/EBPß is a direct target of miR-92b and contributes to its effects on proliferation and differentiation. 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genetics</topic><topic>Antigens, Neoplasm - metabolism</topic><topic>Biology</topic><topic>Cancer</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>CCAAT-Enhancer-Binding Protein-beta - genetics</topic><topic>CCAAT-Enhancer-Binding Protein-beta - metabolism</topic><topic>Cell Adhesion Molecules - genetics</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Proliferation</topic><topic>Cells, Cultured</topic><topic>Correlation analysis</topic><topic>Deregulation</topic><topic>Differentiation</topic><topic>DNA microarrays</topic><topic>Drinking water</topic><topic>Epithelial Cell Adhesion Molecule</topic><topic>Fetus - cytology</topic><topic>Fetus - metabolism</topic><topic>Fetuses</topic><topic>Flow cytometry</topic><topic>Function analysis</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Genes</topic><topic>Genetic transformation</topic><topic>Hepatocytes</topic><topic>Hepatocytes - 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Although recent evidences have been indicated that their aberrant expression may play an important role in cancer stem cells, the mechanism of their deregulation in neoplastic transformation of liver cancer stem cells (LCSCs) has not been explored. In our study, the HCC model was established in F344 rats by DEN induction. The EpCAM(+) cells were sorted out from unfractionated fetal liver cells and liver cancer cells using the FACS analysis and miRNA expression profiles of two groups were screened through microarray platform. Gain-of-function studies were performed in vitro and in vivo to determine the role of miR-92b on proliferation and differentiation of the hepatic progenitors. In addition, luciferase reporter system and gene function analysis were used to predict miR-92b target. we found that miR-92b was highly downregulated in EpCAM(+) fetal liver cells in expression profiling studies. RT-PCR analysis demonstrated reverse correlation between miR-92b expression and differentiation degree in human HCC samples. Overexpression of miR-92b in EpCAM(+) fetal liver cells significantly increased proliferation and inhibited differentiation as well as in vitro and in vivo studies. Moreover, we verified that C/EBPß is a direct target of miR-92b and contributes to its effects on proliferation and differentiation. We conclude that aberrant expression of miR-92b can result in proliferation increase and differentiation arrest of hepatic progenitors by targeting C/EBPß.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23936298</pmid><doi>10.1371/journal.pone.0068004</doi><oa>free_for_read</oa></addata></record>
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subjects Aberration
Analysis
Animals
Antigens, Neoplasm - genetics
Antigens, Neoplasm - metabolism
Biology
Cancer
Carcinoma, Hepatocellular - genetics
Carcinoma, Hepatocellular - metabolism
Carcinoma, Hepatocellular - pathology
CCAAT-Enhancer-Binding Protein-beta - genetics
CCAAT-Enhancer-Binding Protein-beta - metabolism
Cell Adhesion Molecules - genetics
Cell Adhesion Molecules - metabolism
Cell cycle
Cell growth
Cell Proliferation
Cells, Cultured
Correlation analysis
Deregulation
Differentiation
DNA microarrays
Drinking water
Epithelial Cell Adhesion Molecule
Fetus - cytology
Fetus - metabolism
Fetuses
Flow cytometry
Function analysis
Gene expression
Gene Expression Profiling
Genes
Genetic transformation
Hepatocytes
Hepatocytes - cytology
Hepatocytes - metabolism
Humans
Hypotheses
In vivo methods and tests
Laboratory animals
Liver
Liver cancer
Liver Neoplasms - genetics
Liver Neoplasms - metabolism
Liver Neoplasms - pathology
Liver transplants
Male
Medicine
MicroRNA
MicroRNAs
MicroRNAs - genetics
MicroRNAs - metabolism
miRNA
Neoplastic Stem Cells - metabolism
Neoplastic Stem Cells - pathology
Oligonucleotide Array Sequence Analysis
Polymerase chain reaction
Rats
Rats, Inbred F344
Reverse Transcriptase Polymerase Chain Reaction
Ribonucleic acid
RNA
Rodents
Signal transduction
Stem cells
Surgery
Transformation
Up-Regulation
title Upregulated microRNA-92b regulates the differentiation and proliferation of EpCAM-positive fetal liver cells by targeting C/EBPß
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