Abstract |
THAP11 is an essential factor involved in ES cell pluripotency and cell growth. Here, we identified THAP11 as a novel physiological binding partner of PCBP1. In HepG2 cells, THAP11 overexpression inhibited CD44 v6 expression and cell invasion. However, when deleting the binding domain with PCBP1 or endogenous PCBP1 was knocked down, THAP11 failed to inhibit CD44 v6 expression, indicating that THAP11 regulates CD44 v6 expression through interacting with PCBP1. In HCC patients, the expression of THAP11 mRNA significantly correlated with PCBP1 mRNA expression. Our results suggest a novel role of THAP11 in CD44 alternative splicing and hepatoma invasion.
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Authors | Wen-Xi Lian, Rong-Hua Yin, Xiang-Zhen Kong, Tong Zhang, Xian-Hong Huang, Wei-Wei Zheng, Yang Yang, Yi-Qun Zhan, Wang-Xiang Xu, Miao Yu, Chang-Hui Ge, Jun-Tang Guo, Chang-Yan Li, Xiao-Ming Yang |
Journal | FEBS letters
(FEBS Lett)
Vol. 586
Issue 10
Pg. 1431-8
(May 21 2012)
ISSN: 1873-3468 [Electronic] England |
PMID | 22673507
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. |
Chemical References |
- DNA-Binding Proteins
- Heterogeneous-Nuclear Ribonucleoproteins
- Hyaluronan Receptors
- PCBP1 protein, human
- RNA, Messenger
- RNA-Binding Proteins
- Repressor Proteins
- THAP11 protein, human
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Topics |
- Alternative Splicing
- Carcinoma, Hepatocellular
(metabolism, pathology)
- Cell Line, Tumor
- DNA-Binding Proteins
- Gene Knockdown Techniques
- Heterogeneous-Nuclear Ribonucleoproteins
(genetics, metabolism)
- Humans
- Hyaluronan Receptors
(metabolism)
- Liver Neoplasms
(metabolism, pathology)
- Neoplasm Invasiveness
- Protein Binding
- RNA, Messenger
(genetics)
- RNA-Binding Proteins
- Real-Time Polymerase Chain Reaction
- Repressor Proteins
(genetics, metabolism, physiology)
- Reverse Transcriptase Polymerase Chain Reaction
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