Document Detail


Ovarian cancer-derived lysophosphatidic acid stimulates secretion of VEGF and stromal cell-derived factor-1 alpha from human mesenchymal stem cells.
MedLine Citation:
PMID:  20177148     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Lysophosphatidic acid (LPA) stimulates growth and invasion of ovarian cancer cells and tumor angiogenesis. Cancer-derived LPA induces differentiation of human adipose tissue-derived mesenchymal stem cells (hASCs) to alpha-smooth muscle actin (alpha-SMA)-positive cancer-associated fibroblasts. Presently, we explored whether cancer-derived LPA regulates secretion of pro-angiogenic factors from hASCs. Conditioned medium (CM) from the OVCAR-3 and SKOV3 ovarian cancer cell lines stimulated secretion angiogenic factors such as stromal-derived factor-1 alpha (SDF-1 alpha) and VEGF from hASCs. Pretreatment with the LPA receptor inhibitor Ki16425 or short hairpin RNA lentiviral silencing of the LPA((1)) receptor abrogated the cancer CM-stimulated expression of alpha-SMA, SDF-1, and VEGF from hASCs. LPA induced expression of myocardin and myocardin-related transcription factor-A, transcription factors involved in smooth muscle differentiation, in hASCs. siRNA-mediated depletion of endogenous myocardin and MRTF-A abrogated the expression of alpha-SMA, but not SDF-1 and VEGF. LPA activated RhoA in hASCs and pretreatment with the Rho kinase inhibitor Y27632 completely abrogated the LPA-induced expression of alpha-SMA, SDF-1, and VEGF in hASCs. Moreover, LPA-induced alpha-SMA expression was abrogated by treatment with the ERK inhibitor U0126 or the phosphoinositide-3-kinase inhibitor LY294002, but not the PLC inhibitor U73122. LPA-induced VEGF secretion was inhibited by LY294002, whereas LPA-induced SDF-1 secretion was markedly attenuated by U0126, U73122, and LY294002. These results suggest that cancer-secreted LPA induces differentiation of hASCs to cancer-associated fibroblasts through multiple signaling pathways involving Rho kinase, ERK, PLC, and phosphoinositide-3-kinase.
Authors:
Eun Su Jeon; Soon Chul Heo; Il Hwan Lee; Yoon Ji Choi; Ji Hye Park; Kyung Un Choi; Do Youn Park; Dong Soo Suh; Man Soo Yoon; Jae Ho Kim
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Experimental & molecular medicine     Volume:  42     ISSN:  1226-3613     ISO Abbreviation:  Exp. Mol. Med.     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-04-29     Completed Date:  2010-09-20     Revised Date:  2010-09-28    
Medline Journal Info:
Nlm Unique ID:  9607880     Medline TA:  Exp Mol Med     Country:  Korea (South)    
Other Details:
Languages:  eng     Pagination:  280-93     Citation Subset:  IM    
Affiliation:
Medical Research Center for Ischemic Tissue Regeneration, Medical Research Institute, School of Medicine, Pusan National University, Yangsan 626-870, Korea.
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MeSH Terms
Descriptor/Qualifier:
Actins / metabolism
Adipose Tissue / cytology
Cell Line, Tumor
Chemokine CXCL12 / secretion*
Culture Media, Conditioned
Endothelial Cells / drug effects,  metabolism
Female
Humans
Lysophospholipids / pharmacology*
Mesenchymal Stem Cells / drug effects*,  secretion*
Microphthalmia-Associated Transcription Factor / metabolism
Neovascularization, Physiologic / drug effects
Ovarian Neoplasms / enzymology,  metabolism*,  pathology
Paracrine Communication / drug effects
Receptors, Lysophosphatidic Acid / metabolism
Signal Transduction / drug effects
Vascular Endothelial Growth Factors / secretion*
rho-Associated Kinases / metabolism
rhoA GTP-Binding Protein / metabolism
Chemical
Reg. No./Substance:
0/Actins; 0/Chemokine CXCL12; 0/Culture Media, Conditioned; 0/Lysophospholipids; 0/MITF protein, human; 0/Microphthalmia-Associated Transcription Factor; 0/Receptors, Lysophosphatidic Acid; 0/Vascular Endothelial Growth Factors; 22002-87-5/lysophosphatidic acid; EC 2.7.11.1/rho-Associated Kinases; EC 3.6.5.2/rhoA GTP-Binding Protein
Comments/Corrections

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