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2015 ; 8
(9
): 10394-402
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Knockdown of CUL4B inhibits proliferation and promotes apoptosis of colorectal
cancer cells through suppressing the Wnt/?-catenin signaling pathway
#MMPMID26617747
Song B
; Zhan H
; Bian Q
; Li J
Int J Clin Exp Pathol
2015[]; 8
(9
): 10394-402
PMID26617747
show ga
Colorectal cancer is one of the leading causes of cancer related deaths
worldwide. Cullin 4B (CUL4B) is over-expressed in diverse cancer types. However,
the function and precise molecular mechanism of CUL4B in colorectal cancer
remains largely unknown. Therefore, in this study, we examined the expression of
CUL4B in colorectal cancer cell lines and its effects on cellular proliferation
and apoptosis, and the underlying mechanism was also explored. Our results showed
that CUL4B was significantly overexpressed in colorectal cancer cell lines.
Silencing CUL4B obviously inhibited proliferation and tumorigenicity of
colorectal cancer cells both in vitro and in vivo, and it also promoted the
apoptosis of colorectal cancer cells. Moreover, knockdown of CUL4B inhibited the
expression of ?-catenin, cyclin D1 and c-Myc in colorectal cancer cells. Taken
together, these results showed that knockdown of CUL4B inhibit proliferation and
promotes apoptosis of colorectal cancer cells through suppressing the
Wnt/?-catenin signaling pathway. Therefore, CUL4B may represent a novel
therapeutic target for colorectal cancer treatment.