TH
AP11 is an essential factor involved in ES cell pluripotency and cell growth. Here, we identified THAP
11 as a novel physiological binding partner of PCBP
1. In HepG2 cells, THAP
11 overexpression inhibited CD44 v6 expression and cell invasion. However, when deleting the binding domain with PCBP
1 or endogenous PCBP
1 was knocked down, THAP
11 failed to inhibit CD44 v6 expression, indicating that THAP
11 regulates CD44 v6 expression through interacting with PCBP
1. In HCC patients, the expression of THAP
11 mRNA significantly correlated with PCBP
1 mRNA expression. Our results suggest a novel role of THAP
11 in CD44 alternative splicing and hepatoma invasion.
Structured summary of protein interactions:
with by () with by (View Interaction: , ) and by ()