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The stress response gene ATF3 is a direct target of the Wnt/?-catenin pathway and
inhibits the invasion and migration of HCT116 human colorectal cancer cells
#MMPMID29966001
Inoue M
; Uchida Y
; Edagawa M
; Hirata M
; Mitamura J
; Miyamoto D
; Taketani K
; Sekine S
; Kawauchi J
; Kitajima S
PLoS One
2018[]; 13
(7
): e0194160
PMID29966001
show ga
Aberrant Wnt/?-catenin signaling is implicated in tumorigenesis and the
progression of human colorectal cancers, and mutations in the components of the
Wnt/?-catenin signaling pathway are observed in the majority of patients.
Therefore, extensive studies on the Wnt signaling pathway and its target genes
are crucial to understand the molecular events of tumorigenesis and develop an
efficacious therapy. In this study, we showed that the stress response gene ATF3
is transcriptionally activated by the binding of ?-catenin and TCF4 to the
redundant TCF4 site at the proximal promoter region of the ATF3 gene, indicating
that ATF3 is a direct target of the Wnt/?-catenin pathway. The loss of function
or overexpression studies showed that ATF3 inhibited the migration or invasion of
HCT116 cells. The expression of some MMP and TIMP genes and the ratio of MMP2/9
to TIMP3/4 mRNAs was differentially regulated by ATF3. Therefore, though ATF3 is
activated downstream of the Wnt/?-catenin pathway, it acts as a negative
regulator of the migration and invasion of HCT116 human colon cancer cells
exhibiting aberrant Wnt/?-catenin activity. ATF3 is a candidate biomarker and
target for human colorectal cancer treatment and prevention.
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