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2017 ; 10
(ä): 2609-2619
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RNA-binding protein HuR promotes bladder cancer progression by competitively
binding to the long noncoding HOTAIR with miR-1
#MMPMID28553126
Yu D
; Zhang C
; Gui J
Onco Targets Ther
2017[]; 10
(ä): 2609-2619
PMID28553126
show ga
The elevated expressions of RNA-binding protein HuR and long noncoding HOX
transcript antisense RNA (HOTAIR) are observed in numerous cancers. And HuR often
exerts its promotive effects on tumorigenesis via binding to AU-rich elements in
target transcripts and thus regulating the expression of target transcripts.
However, the roles and related mechanisms of HuR/HOTAIR in bladder cancer
progression have never been formally tested. Here, we found that the expression
level of HuR was higher in clinical bladder cancer samples than in normal
adjacent samples, mirroring that of HOTAIR, and their expression showed strong
correlation. Knockdown of HuR/HOTAIR in bladder cancer inhibited cell
proliferation, migration, invasion, and promoted cell apoptosis. Notably, HuR
interacted and stabilized HOTAIR mRNA and knockdown of HuR decreased HOTAIR
expression. Additionally, HOTAIR was identified as a potential target of miR-1 in
bladder cancer cells. Interestingly, overexpression of HOTAIR enhanced HuR
expression and increased cytoplasmic accumulation of HuR, thus enhancing HOTAIR
expression in turn. But mutation of miR-1 binding site in HOTAIR canceled the
effects of HOTAIR on HuR expression. Overall, we identified a regulatory loop
between HOTAIR and HuR during the progression of bladder cancer, which could be
exploited to curb bladder cancer progression.