Genome-wide pattern of TCF7L2/TCF4 chromatin occupancy in colorectal cancer cells.

P. Hatzis; L.G. van der Flier; M.A. van Driel; V. Guryev; F. Nielsen; S. Denissov; I.J. Nijman; J. Koster; E.E. Santo; W. Welboren; R. Versteeg; M.L. van de Wetering; H. Clevers; H.G. Stunnenberg

doi:10.1128/MCB.02175-07

Genome-wide pattern of TCF7L2/TCF4 chromatin occupancy in colorectal cancer cells.

P. Hatzis, L.G. van der Flier, M.A. van Driel, V. Guryev, F. Nielsen, S. Denissov, I.J. Nijman, J. Koster, E.E. Santo, W. Welboren, R. Versteeg, M.L. van de Wetering, H. Clevers, H.G. Stunnenberg

Hubrecht Institute

Research output: Contribution to journal/periodical › Article › Scientific › peer-review

199 Citations (Scopus)

Abstract

Wnt signaling activates gene expression through the induced formation of complexes between DNA-binding T-cell factors (TCFs) and the transcriptional coactivator beta-catenin. In colorectal cancer, activating Wnt pathway mutations transform epithelial cells through the inappropriate activation of a TCF7L2/TCF4 target gene program. Through a DNA array-based genome-wide analysis of TCF4 chromatin occupancy, we have identified 6,868 high-confidence TCF4-binding sites in the LS174T colorectal cancer cell line. Most TCF4-binding sites are located at large distances from transcription start sites, while target genes are frequently "decorated" by multiple binding sites. Motif discovery algorithms define the in vivo-occupied TCF4-binding site as evolutionarily conserved A-C/G-A/T-T-C-A-A-A-G motifs. The TCF4-binding regions significantly correlate with Wnt-responsive gene expression profiles derived from primary human adenomas and often behave as beta-catenin/TCF4-dependent enhancers in transient reporter assays.

Original language	English
Pages (from-to)	2732-2744
Journal	Molecular and Cellular Biology
Volume	28
Issue number	8
DOIs	https://doi.org/10.1128/MCB.02175-07
Publication status	Published - 2008

Access to Document

10.1128/MCB.02175-07

Cite this

Hatzis, P., van der Flier, L. G., van Driel, M. A., Guryev, V., Nielsen, F., Denissov, S., Nijman, I. J., Koster, J., Santo, E. E., Welboren, W., Versteeg, R., van de Wetering, M. L., Clevers, H., & Stunnenberg, H. G. (2008). Genome-wide pattern of TCF7L2/TCF4 chromatin occupancy in colorectal cancer cells. Molecular and Cellular Biology, 28(8), 2732-2744. https://doi.org/10.1128/MCB.02175-07

@article{f071960d15f1493a9a089b1568e7aa3d,

title = "Genome-wide pattern of TCF7L2/TCF4 chromatin occupancy in colorectal cancer cells.",

abstract = "Wnt signaling activates gene expression through the induced formation of complexes between DNA-binding T-cell factors (TCFs) and the transcriptional coactivator beta-catenin. In colorectal cancer, activating Wnt pathway mutations transform epithelial cells through the inappropriate activation of a TCF7L2/TCF4 target gene program. Through a DNA array-based genome-wide analysis of TCF4 chromatin occupancy, we have identified 6,868 high-confidence TCF4-binding sites in the LS174T colorectal cancer cell line. Most TCF4-binding sites are located at large distances from transcription start sites, while target genes are frequently {"}decorated{"} by multiple binding sites. Motif discovery algorithms define the in vivo-occupied TCF4-binding site as evolutionarily conserved A-C/G-A/T-T-C-A-A-A-G motifs. The TCF4-binding regions significantly correlate with Wnt-responsive gene expression profiles derived from primary human adenomas and often behave as beta-catenin/TCF4-dependent enhancers in transient reporter assays.",

author = "P. Hatzis and {van der Flier}, L.G. and {van Driel}, M.A. and V. Guryev and F. Nielsen and S. Denissov and I.J. Nijman and J. Koster and E.E. Santo and W. Welboren and R. Versteeg and {van de Wetering}, M.L. and H. Clevers and H.G. Stunnenberg",

note = "Reporting year: 2008",

year = "2008",

doi = "10.1128/MCB.02175-07",

language = "English",

volume = "28",

pages = "2732--2744",

journal = "Molecular and Cellular Biology",

issn = "0270-7306",

publisher = "American Society for Microbiology",

number = "8",

}

Hatzis, P, van der Flier, LG, van Driel, MA, Guryev, V, Nielsen, F, Denissov, S, Nijman, IJ, Koster, J, Santo, EE, Welboren, W, Versteeg, R, van de Wetering, ML, Clevers, H & Stunnenberg, HG 2008, 'Genome-wide pattern of TCF7L2/TCF4 chromatin occupancy in colorectal cancer cells.', Molecular and Cellular Biology, vol. 28, no. 8, pp. 2732-2744. https://doi.org/10.1128/MCB.02175-07

TY - JOUR

T1 - Genome-wide pattern of TCF7L2/TCF4 chromatin occupancy in colorectal cancer cells.

AU - Hatzis, P.

AU - van der Flier, L.G.

AU - van Driel, M.A.

AU - Guryev, V.

AU - Nielsen, F.

AU - Denissov, S.

AU - Nijman, I.J.

AU - Koster, J.

AU - Santo, E.E.

AU - Welboren, W.

AU - Versteeg, R.

AU - van de Wetering, M.L.

AU - Clevers, H.

AU - Stunnenberg, H.G.

N1 - Reporting year: 2008

PY - 2008

Y1 - 2008

N2 - Wnt signaling activates gene expression through the induced formation of complexes between DNA-binding T-cell factors (TCFs) and the transcriptional coactivator beta-catenin. In colorectal cancer, activating Wnt pathway mutations transform epithelial cells through the inappropriate activation of a TCF7L2/TCF4 target gene program. Through a DNA array-based genome-wide analysis of TCF4 chromatin occupancy, we have identified 6,868 high-confidence TCF4-binding sites in the LS174T colorectal cancer cell line. Most TCF4-binding sites are located at large distances from transcription start sites, while target genes are frequently "decorated" by multiple binding sites. Motif discovery algorithms define the in vivo-occupied TCF4-binding site as evolutionarily conserved A-C/G-A/T-T-C-A-A-A-G motifs. The TCF4-binding regions significantly correlate with Wnt-responsive gene expression profiles derived from primary human adenomas and often behave as beta-catenin/TCF4-dependent enhancers in transient reporter assays.

AB - Wnt signaling activates gene expression through the induced formation of complexes between DNA-binding T-cell factors (TCFs) and the transcriptional coactivator beta-catenin. In colorectal cancer, activating Wnt pathway mutations transform epithelial cells through the inappropriate activation of a TCF7L2/TCF4 target gene program. Through a DNA array-based genome-wide analysis of TCF4 chromatin occupancy, we have identified 6,868 high-confidence TCF4-binding sites in the LS174T colorectal cancer cell line. Most TCF4-binding sites are located at large distances from transcription start sites, while target genes are frequently "decorated" by multiple binding sites. Motif discovery algorithms define the in vivo-occupied TCF4-binding site as evolutionarily conserved A-C/G-A/T-T-C-A-A-A-G motifs. The TCF4-binding regions significantly correlate with Wnt-responsive gene expression profiles derived from primary human adenomas and often behave as beta-catenin/TCF4-dependent enhancers in transient reporter assays.

U2 - 10.1128/MCB.02175-07

DO - 10.1128/MCB.02175-07

M3 - Article

SN - 0270-7306

VL - 28

SP - 2732

EP - 2744

JO - Molecular and Cellular Biology

JF - Molecular and Cellular Biology

IS - 8

ER -

Genome-wide pattern of TCF7L2/TCF4 chromatin occupancy in colorectal cancer cells.

Abstract

Access to Document

Fingerprint

Cite this