Document Detail


Alpha-fetoprotein: a new member of intracellular signal molecules in regulation of the PI3K/AKT signaling in human hepatoma cell lines.
MedLine Citation:
PMID:  20473866     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Despite its well-defined role as a serum growth factor during fetal liver development and hepatic oncogenesis, the biological significance of cytoplasmic alpha-fetoprotein (AFP) remains incompletely understood. Here, we provide evidence to illustrate that cytoplasmic AFP may function as a regulator in the phosphatidylinositol 3-kinase (PI3K)/AKT pathway in human hepatocellular carcinoma cells. The results demonstrated colocalization and interaction of AFP and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in the cytoplasm of AFP-producing Bel 7402 and HepG2 cells, with an interaction distance of 12.6 ± 2.7 Å as determined with the fluorescence resonance energy transfer technique. Knockdown of AFP mRNA or inhibition of AFP expression by all trans-retinoic acid resulted in enhancement of the PTEN level with a synchronous decrease in phosphorylated AKT. Transfection of the afp gene into HLE cells (originally AFP negative) led to a significant activation of AKT signaling. The inhibition of PI3K signaling by LY 294002 was simultaneously reversed by transfection, accompanied by diminution of all trans-retinoic acid-induced upregulation of PTEN and enhancement of cell growth. In conclusion, these results demonstrate that cytoplasmic AFP is involved in regulation of hepatocellular growth and tumorigenesis.
Authors:
Mengsen Li; Hui Li; Chaoying Li; Shanshan Wang; Wei Jiang; Zhongmin Liu; Sheng Zhou; Xinhua Liu; Michael A McNutt; Gang Li
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of cancer. Journal international du cancer     Volume:  128     ISSN:  1097-0215     ISO Abbreviation:  Int. J. Cancer     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2010-11-29     Completed Date:  2011-01-14     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0042124     Medline TA:  Int J Cancer     Country:  United States    
Other Details:
Languages:  eng     Pagination:  524-32     Citation Subset:  IM    
Affiliation:
Key Laboratory of Molecular Biology, Hainan Medical College, Haikou, Hainan, China.
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MeSH Terms
Descriptor/Qualifier:
Carcinoma, Hepatocellular / genetics,  metabolism*,  pathology
Cell Adhesion Molecules / deficiency
Chromosomes, Human, Pair 10
Fluorescence Resonance Energy Transfer
Gene Deletion
Homeostasis
Humans
Liver Neoplasms / genetics,  metabolism*,  pathology
Microfilament Proteins / deficiency
PTEN Phosphohydrolase / genetics,  metabolism
Proto-Oncogene Proteins c-akt / genetics,  metabolism*
RNA Interference
Signal Transduction
Transfection
Tretinoin / pharmacology
Tumor Suppressor Proteins / genetics,  metabolism
Up-Regulation
alpha-Fetoproteins / genetics,  physiology*
Chemical
Reg. No./Substance:
0/Cell Adhesion Molecules; 0/Microfilament Proteins; 0/Tumor Suppressor Proteins; 0/alpha-Fetoproteins; 0/tensins; 302-79-4/Tretinoin; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 3.1.3.48/PTEN protein, human; EC 3.1.3.67/PTEN Phosphohydrolase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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