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Peroxiredoxin 2 is essential for maintaining cancer stem cell-like phenotype
through activation of Hedgehog signaling pathway in colon cancer
#MMPMID27894099
Wang R
; Wei J
; Zhang S
; Wu X
; Guo J
; Liu M
; Du K
; Xu J
; Peng L
; Lv Z
; You W
; Xiong Y
; Fu Z
Oncotarget
2016[Dec]; 7
(52
): 86816-86828
PMID27894099
show ga
Cancer stem cells (CSCs) are a key target for reducing tumor growth, metastasis,
and recurrence. Redox status is a critical factor in the maintenance of CSCs, and
the antioxidant enzyme Peroxiredoxin 2 (Prdx2) plays an important role in the
development of colon cancer. Therefore, we investigated the contribution of Prdx2
to the maintenance of stemness of colon CSCs. Here, we used short-hairpin RNAs
and a Prdx2-overexpression vector to determine the effects of Prdx2. We
demonstrated that knockdown of Prdx2 reduced the self-renewal and sphere
formation and resulted in increased 5-FU-induced apoptosis in human colon CSCs.
Prdx2 overexpression induced reversion of the self-renewal and sphere formation.
Furthermore, the effects of Prdx2 resulted in an altered expression of stemness
associated with the Hh/Gli1 signaling pathway. Finally, knockdown of Prdx2 in
CD133+ cells reduced the volume of xenograft tumors in BALB/c-nu mice. Taken
together, colon CSCs overexpress Prdx2, which promotes their stem cell properties
via the Hh/Gli1 signaling pathway. The results suggest that Prdx2 may be an
effective therapeutic target for the elimination of CSCs in colorectal cancer.
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