Facilitates Chromatin Transcription Complex Is an "Accelerator" of Tumor Transformation and Potential Marker and Target of Aggressive Cancers Journal Article


Authors: Garcia, H.; Miecznikowski, J. C.; Safina, A.; Commane, M.; Ruusulehto, A.; Kilpinen, S.; Leach, R. W.; Attwood, K.; Li, Y.; Degan, S.; Omilian, A. R.; Guryanova, O.; Papantonopoulou, O.; Wang, J.; Buck, M.; Liu, S.; Morrison, C.; Gurova, K. V.
Article Title: Facilitates Chromatin Transcription Complex Is an "Accelerator" of Tumor Transformation and Potential Marker and Target of Aggressive Cancers
Abstract: The facilitates chromatin transcription (FACT) complex is involved in chromatin remodeling during transcription, replication, and DNA repair. FACT was previously considered to be ubiquitously expressed and not associated with any disease. However, we discovered that FACT is the target of a class of anticancer compounds and is not expressed in normal cells of adult mammalian tissues, except for undifferentiated and stem-like cells. Here, we show that FACT expression is strongly associated with poorly differentiated aggressive cancers with low overall survival. In addition, FACT was found to be upregulated during invitro transformation and to be necessary, but not sufficient, for driving transformation. FACT also promoted survival and growth of established tumor cells. Genome-wide mapping of chromatin-bound FACT indicated that FACT's role in cancer most likely involves selective chromatin remodeling of genes that stimulate proliferation, inhibit cell death and differentiation, and regulate cellular stress responses. © 2013 The Authors.
Keywords: cancer survival; controlled study; protein expression; survival rate; unclassified drug; major clinical study; overall survival; sequence analysis; dna-binding proteins; clinical feature; cancer growth; nonhuman; disease marker; protein function; biological marker; animal cell; mouse; mammalia; animals; cell cycle proteins; mice; animal tissue; complex formation; molecular dynamics; animal experiment; animal model; genetic association; genetic transcription; in vivo study; cell differentiation; transcription, genetic; mice, scid; mice, inbred c57bl; transcription factors; cell transformation, neoplastic; gene expression regulation, neoplastic; chromatin; nucleotide sequence; tumor protein; malignant neoplastic disease; dna sequence; cellular stress response; malignant transformation; protein determination; mcf-7 cells; genome, human; chromatin assembly and disassembly; transcriptional elongation factors; molecular pathology; disease activity; high mobility group proteins; humans; human; priority journal; article; facilitate chromatin transcription complex protein
Journal Title: Cell Reports
Volume: 4
Issue: 1
ISSN: 2211-1247
Publisher: Cell Press  
Date Published: 2013-07-11
Start Page: 159
End Page: 173
Language: English
DOI: 10.1016/j.celrep.2013.06.013
PUBMED: 23831030
PROVIDER: scopus
PMCID: PMC5886782
DOI/URL:
Notes: Export Date: 9 May 2014 -- Molecular Sequence Numbers: GENBANK: GSE45393; -- Source: Scopus
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