Document Detail

Proteomic snapshot of breast cancer cell cycle: G1/S transition point.
MedLine Citation:
PMID:  23152136     Owner:  NLM     Status:  MEDLINE    
The biological processes that unfold during the G1-phase of the cell cycle are dependent on extracellular mitogenic factors that signal the cell to enter a state of quiescence, or commit to a cell-cycle round by passing the restriction point (R-point) and enter the S-phase. Unlike normal cells, cancer cells evolved the ability to evade the R-point and continue through the cell cycle even in the presence of extensive DNA damage or absence of mitogenic signals. The purpose of this study was to perform a quantitative proteomic evaluation of the biological processes that are responsible for driving MCF-7 breast cancer cells into division even when molecular checkpoints such as the G1/S R-point are in place. Nuclear and cytoplasmic fractions of the G1 and S cell-cycle phases were analyzed by LC-MS/MS to result in the confident identification of more than 2700 proteins. Statistical evaluation of the normalized data resulted in the selection of proteins that displayed twofold or more change in spectral counts in each cell state. Pathway mapping, functional annotation clustering, and protein interaction network analysis revealed that the top-scoring clusters that could play a role in overriding the G1/S transition point included DNA damage response, chromatin remodeling, transcription/translation regulation, and signaling proteins.
Milagros J Tenga; Iulia M Lazar
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Proteomics     Volume:  13     ISSN:  1615-9861     ISO Abbreviation:  Proteomics     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-01-11     Completed Date:  2013-06-19     Revised Date:  2014-08-10    
Medline Journal Info:
Nlm Unique ID:  101092707     Medline TA:  Proteomics     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  48-60     Citation Subset:  IM    
Copyright Information:
© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
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MeSH Terms
Breast Neoplasms* / genetics,  metabolism,  pathology
Cell Cycle / genetics
Cell Nucleolus / metabolism
Chromatin Assembly and Disassembly / genetics
Cytoplasm / metabolism
DNA Damage / genetics
G1 Phase Cell Cycle Checkpoints / genetics*
MCF-7 Cells
Neoplasm Proteins* / biosynthesis,  genetics,  metabolism
Proteome / analysis*
Signal Transduction / genetics
Transcription, Genetic / genetics
Grant Support
R21 CA126669/CA/NCI NIH HHS; R21 CA126669-01A1/CA/NCI NIH HHS
Reg. No./Substance:
0/Neoplasm Proteins; 0/Proteome

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

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