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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Cancer+Biol+Ther
2014 ; 15
(9
): 1174-84
Nephropedia Template TP
gab.com Text
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QKI impairs self-renewal and tumorigenicity of oral cancer cells via repression
of SOX2
#MMPMID24918581
Lu W
; Feng F
; Xu J
; Lu X
; Wang S
; Wang L
; Lu H
; Wei M
; Yang G
; Wang L
; Lu Z
; Liu Y
; Lei X
Cancer Biol Ther
2014[Sep]; 15
(9
): 1174-84
PMID24918581
show ga
Cancer stem cells (CSCs) may contribute to tumor initiation, distant metastasis
and chemo-resistance. One of RNA-binding proteins, Quaking (QKI), was reported to
be a tumor suppressor. Here we showed that reduced QKI levels were observed in
many human oral cancer samples. Moreover further reduction of QKI expression in
CSCs was detected compared with non-CSCs in oral cancer cell lines.
Overexpressing QKI in oral cancer cells significantly reduced CSC sphere
formation and stem cell-associated genes. In tumor implanting nude mice model,
QKI significantly impeded tumor initiation rates, tumor sizes and lung metastasis
rates. As a contrast, knocking down QKI enhanced the above effects. Among the
putative CSC target genes, SOX2 expression was negatively affected by QKI,
mechanism study revealed that QKI may directly regulate SOX2 expression via
specific binding with its 3'UTR in a cis element-dependent way. Loss of SOX2 even
completely reversed the sphere forming ability in QKI knockdown cell line. Taken
together, these data demonstrated that SOX2 is an important CSC regulator in oral
cancer. QKI is a novel CSC inhibitor and impaired multiple oral CSC properties
via partial repression of SOX2. Therefore, reduced expression of QKI may provide
a novel diagnostic marker for oral cancer.