Document Detail


Toll-like receptor-4 agonist inhibits motility and invasion of hepatoblastoma HepG2 cells in vitro.
MedLine Citation:
PMID:  22648929     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
BACKGROUND: Expression of toll-like receptor-4 (TLR4) on tumor cells is known to mediate innate immune responses that influence tumor cell growth and migration. This study aimed to characterize TLR4 expression and elucidate its functional significance in human hepatoblastoma (HB) cells. PROCEDURE: Immunohistochemistry (IHC) was used to determine TLR4 expression level and its distribution pattern in HB liver tissues. Transcripts of tumor necrosis factor (TNF)-α, interleukin (IL)-8, matrix metalloproteinase (MMP)-2, MMP-13, tissue inhibitor of metalloproteinases (TIMP)-1, and TIMP-2 in HB HepG2 cells with lipopolysacharide (LPS) treatment were measured by quantitative PCR. Soluble cytokines and peptides in conditioned media were measured by ELISA. MMP-2 activity was determined by using gelatin zymography. Cell motility and invasiveness was determined using wound healing migration and Matrigel invasion assays, respectively. RESULTS: TLR4 IHC staining demonstrated that TLR4 overexpression in HB liver tissues dramatically vanished after chemotherapy. In vitro study using an HB cell line, HepG2, showed that TLR4 agonist, LPS, significantly decreased transcripts of IL-8 and TNF-α, but did not affect MMP-13 mRNA level. By contrast, LPS only down-regulated IL-8 production and MMP-2 gelatinolytic activity. The latter might be in part due to the increased levels of MMP-2/TIMP-2 complex in conditioned media, thus leading to the decreased motility and invasiveness of HepG2 cells. CONCLUSIONS: HB cells overexpress TLR4, whereas TLR4 agonistic treatment inhibits migration and invasion of HB HepG2 cells. These findings suggest that TLR4 signaling pathway is a potential therapeutic target for control of HB tumor progression. Pediatr Blood Cancer © 2012 Wiley Periodicals, Inc.
Authors:
Chih-Cheng Hsiao; Ying-Hsien Kao; Shun-Chen Huang; Jiin-Haur Chuang
Related Documents :
20125039 - Discriminant model for cytologic distinction of large cell neuroendocrine carcinoma fro...
521539 - Cell proliferation in a malignant angioendothelioma during sequential chemotherapy.
19700179 - A new technique for the diagnosis of mycetoma using fixed blocks of aspirated material.
22751989 - Sirtinol, a class iii hdac inhibitor, induces apoptotic and autophagic cell death in mc...
7686399 - A study of surface property changes in rat mesothelial cells induced by asbestos using ...
6205529 - Rapid identification of glial cells in human amniotic fluid with indirect immunofluores...
15183489 - P53-independent thermosensitization by mitomycin c in human non-small-cell lung cancer ...
23104529 - Presenilin 1 is frequently overexpressed and positively associates with epidermal growt...
25109839 - Spy'ing on differentiation in neuroblastoma.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-5-30
Journal Detail:
Title:  Pediatric blood & cancer     Volume:  -     ISSN:  1545-5017     ISO Abbreviation:  -     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-5-31     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101186624     Medline TA:  Pediatr Blood Cancer     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012 Wiley Periodicals, Inc.
Affiliation:
Division of Hematology/Oncology, Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

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


Previous Document:  Saturation-recovery metabolic-exchange rate imaging with hyperpolarized [1-(13) C] pyruvate using sp...
Next Document:  Lack of Tir Ubiquitylation Contributes to Enteropathogenic E. coli Remaining Extracellular During No...