Notably, the expression level of DDX17 showed a trend (i.e., DDX17 expression in muscle-invasive bladder cancer > DDX17 expression in nonmuscle-invasive bladder cancer > DDX17 expression in control samples) that might be attributed to the fact that the human RNA helicase DDX17 contributes to tumor cell invasiveness by regulating the alternative splicing of several DNA and chromatin-binding factors ( 13 ).
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