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A polymorphic enhancer near GREM1 influences bowel cancer risk through differential CDX2 and TCF7L2 binding.

Abstract：

:A rare germline duplication upstream of the bone morphogenetic protein antagonist GREM1 causes a Mendelian-dominant predisposition to colorectal cancer (CRC). The underlying disease mechanism is strong, ectopic GREM1 overexpression in the intestinal epithelium. Here, we confirm that a common GREM1 polymorphism, rs16969681, is also associated with CRC susceptibility, conferring ∼20% differential risk in the general population. We hypothesized the underlying cause to be moderate differences in GREM1 expression. We showed that rs16969681 lies in a region of active chromatin with allele- and tissue-specific enhancer activity. The CRC high-risk allele was associated with stronger gene expression, and higher Grem1 mRNA levels increased the intestinal tumor burden in Apc(Min) mice. The intestine-specific transcription factor CDX2 and Wnt effector TCF7L2 bound near rs16969681, with significantly higher affinity for the risk allele, and CDX2 overexpression in CDX2/GREM1-negative cells caused re-expression of GREM1. rs16969681 influences CRC risk through effects on Wnt-driven GREM1 expression in colorectal tumors.

journal_name

Cell Rep

journal_title

Cell reports

authors

Lewis A,Freeman-Mills L,de la Calle-Mustienes E,Giráldez-Pérez RM,Davis H,Jaeger E,Becker M,Hubner NC,Nguyen LN,Zeron-Medina J,Bond G,Stunnenberg HG,Carvajal JJ,Gomez-Skarmeta JL,Leedham S,Tomlinson I

doi

10.1016/j.celrep.2014.07.020

subject

Has Abstract

pub_date

2014-08-21 00:00:00

pages

983-90

issue

4

issn

2211-1247

pii

S2211-1247(14)00589-0

journal_volume

8

pub_type

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