Document Detail


Transforming growth factor-β and the hallmarks of cancer.
MedLine Citation:
PMID:  20940046     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Tumorigenesis is in many respects a process of dysregulated cellular evolution that drives malignant cells to acquire six phenotypic hallmarks of cancer, including their ability to proliferate and replicate autonomously, to resist cytostatic and apoptotic signals, and to induce tissue invasion, metastasis, and angiogenesis. Transforming growth factor-β (TGF-β) is a potent pleiotropic cytokine that functions as a formidable barrier to the development of cancer hallmarks in normal cells and tissues. Paradoxically, tumorigenesis counteracts the tumor suppressing activities of TGF-β, thus enabling TGF-β to stimulate cancer invasion and metastasis. Fundamental gaps exist in our knowledge of how malignant cells overcome the cytostatic actions of TGF-β, and of how TGF-β stimulates the acquisition of cancer hallmarks by developing and progressing human cancers. Here we review the molecular and cellular mechanisms that underlie the ability of TGF-β to mediate tumor suppression in normal cells, and conversely, to facilitate cancer progression and disease dissemination in malignant cells.
Authors:
Maozhen Tian; Jason R Neil; William P Schiemann
Related Documents :
20562526 - Tumor cells induce the cancer associated fibroblast phenotype via caveolin-1 degradatio...
19610616 - Combining hit identification strategies: fragment-based and in silico approaches to ora...
16155796 - In vitro and in vivo effects of combination of trastuzumab (herceptin) and tamoxifen in...
12162696 - Geneblocs are powerful tools to study and delineate signal transduction processes that ...
9703786 - Adjuvant radiotherapy in the treatment of breast cancer.
12492466 - Living with breast cancer - a challenge to expansive and creative forces.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review     Date:  2010-11-06
Journal Detail:
Title:  Cellular signalling     Volume:  23     ISSN:  1873-3913     ISO Abbreviation:  Cell. Signal.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-03-22     Completed Date:  2011-06-27     Revised Date:  2014-09-12    
Medline Journal Info:
Nlm Unique ID:  8904683     Medline TA:  Cell Signal     Country:  England    
Other Details:
Languages:  eng     Pagination:  951-62     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Inc. All rights reserved.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Cell Cycle
Cell Movement
Cell Proliferation
Cell Survival
Epithelial-Mesenchymal Transition
Humans
Intracellular Signaling Peptides and Proteins / genetics,  metabolism
Mutation, Missense
Neoplasm Invasiveness
Neoplasms / genetics,  metabolism*,  pathology
Neovascularization, Pathologic / metabolism
Phenotype*
Signal Transduction
Transforming Growth Factor beta / metabolism*
Grant Support
ID/Acronym/Agency:
CA129359/CA/NCI NIH HHS; R01 CA129359/CA/NCI NIH HHS; R01 CA129359-03/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Intracellular Signaling Peptides and Proteins; 0/Transforming Growth Factor beta
Comments/Corrections

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


Previous Document:  JAK2 is an important signal transducer in IL-33-induced NF-?B activation.
Next Document:  Regulation of the CREB coactivator TORC by the dual leucine zipper kinase at different levels.