Document Detail

Growth inhibition induced by transforming growth factor-beta1 in human oral squamous cell carcinoma.
MedLine Citation:
PMID:  18418730     Owner:  NLM     Status:  MEDLINE    
Oral squamous cell carcinoma (OSCC) is a world-wide health problem and its incidence accounts for 1.9-3.5% of all malignant tumors. Transforming growth factor beta/Smads (TGF-beta/Smads) signaling pathway plays an important role in oncogenesis, but its function and molecular mechanisms in OSCC remain unclear. Expression of transforming growth factor-beta receptor type II (TbetaRII) and Smad4 was studied by immunohistochemistry in 108 OSCC patients and 10 normal controls. Function and molecular mechanisms of TGF-beta/Smads signaling pathway was then investigated in two human tongue squamous carcinoma cell lines with high and low metastasis (Tb and Tca8113) by RT-PCR, Western Blot, immunofluorescence, cell growth curve and flow cytometry (FCM), respectively. TbetaRII and Smad4 were significantly down-regulated in tumor tissues (with or without lymph node metastasis) compared to normal oral epithelium tissues (P < 0.05). TGF-beta1 induced arrest of the cell cycle rather than cell death in Tca8113 and Tb cells, and this influence was mediated by the increasing the expression and changing the location of its downstream components of TGF-beta1/Smads signaling pathway. TGF-beta1 rapidly increased the expression of p15 and p21 in both Tca8113 and Tb cells. TGF-beta1 did not increase p27 expression in Tca8113 cells, but p27 expression was increased in Tb cells. These indicated that TGF-beta1 induced G(1) arrest of cell cycle through a different regulating pathway in Tb cells compared with Tca8113 cells. Thus, we conclude that TGF-beta/Smads signaling pathway play a important role on cell growth and metastasis potential in OSCC.
Xiumei Wang; Wenjing Sun; Jing Bai; Linlin Ma; Yang Yu; Jingshu Geng; Jiping Qi; Zhongcheng Shi; Songbin Fu
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-04-17
Journal Detail:
Title:  Molecular biology reports     Volume:  36     ISSN:  1573-4978     ISO Abbreviation:  Mol. Biol. Rep.     Publication Date:  2009 May 
Date Detail:
Created Date:  2009-04-02     Completed Date:  2009-07-23     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0403234     Medline TA:  Mol Biol Rep     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  861-9     Citation Subset:  IM    
The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Carcinoma, Squamous Cell / pathology*
Cell Line, Tumor
Cell Nucleus / drug effects,  metabolism
Cell Proliferation / drug effects
Cyclin-Dependent Kinase Inhibitor p15 / genetics,  metabolism
Cyclin-Dependent Kinase Inhibitor p21 / genetics,  metabolism
Cyclin-Dependent Kinase Inhibitor p27 / genetics,  metabolism
G1 Phase / drug effects
Gene Expression Regulation, Neoplastic / drug effects
Mouth Neoplasms / pathology*
Protein Transport / drug effects
Protein-Serine-Threonine Kinases / metabolism
Receptors, Transforming Growth Factor beta / metabolism
Smad Proteins / genetics,  metabolism
Transforming Growth Factor beta1 / pharmacology*
Reg. No./Substance:
0/Cyclin-Dependent Kinase Inhibitor p15; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Receptors, Transforming Growth Factor beta; 0/Smad Proteins; 0/Transforming Growth Factor beta1; 147604-94-2/Cyclin-Dependent Kinase Inhibitor p27; EC Kinases; EC growth factor-beta type II receptor

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

Previous Document:  Friends and foes: streptomycetes as modulators of plant disease and symbiosis.
Next Document:  Heat shock proteins HSP70 and HSP27 in the cerebral spinal fluid of patients undergoing thoracic ane...