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SIX1 promotes epithelial–mesenchymal transition in colorectal cancer through ZEB1 activation
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SIX1 promotes epithelial–mesenchymal transition in colorectal cancer through ZEB1 activation
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Journal Article
SIX1 promotes epithelial–mesenchymal transition in colorectal cancer through ZEB1 activation
2012
Overview
Epithelial–mesenchymal transition (EMT) has a major role in cancer progression, as well as normal organ development and human pathology such as organ fibrosis and wound healing. Here, we performed a gene expression array specialized in EMT of colorectal cancer (CRC). From a comprehensive gene expression analysis using epithelial- and mesenchymal-like CRC cell lines, and following the ontology (GO) analysis,
SIX1
gene was identified to be an EMT-related gene in CRC. Using SW480 cells stably transfected with a
SIX1
expression construct and their control counterparts, we demonstrated that
SIX1
overexpression represses
CDH1
expression and promotes EMT in CRC.
SIX1
-induced
CDH1
repression and EMT in CRC cells were correlated at least in part with posttranscriptional
ZEB1
activation and
miR-200
-family transcriptional repression. In primary tumors of CRC, in accord with the functional findings, aberrant expression of
SIX1
in cancer cells was observed at the disruption of the basement membrane and at the tumor invasive front, where tumor cells underwent EMT
in vivo
. Taken together,
SIX1
overexpression is suggested to occur in carcinogenesis, and contribute to repression of
CDH1
expression and promotion of EMT partly through repression of
miR-200
-family expression and activation of
ZEB1
in CRC.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Cancer
/ Colorectal Neoplasms - metabolism
/ Colorectal Neoplasms - mortality
/ Colorectal Neoplasms - pathology
/ Epithelial-Mesenchymal Transition - genetics
/ Female
/ Fibrosis
/ Gene Expression Regulation, Neoplastic
/ Homeodomain Proteins - genetics
/ Homeodomain Proteins - metabolism
/ Homeodomain Proteins - physiology
/ Humans
/ Male
/ Medicine
/ Oligonucleotide Array Sequence Analysis
/ Oncology
/ Transcription Factors - genetics
/ Transcription Factors - metabolism
/ Tumors
