Histone H3 lysine 27 trimethylation in adult differentiated colon associated to cancer DNA hypermethylation
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Histone H3 lysine 27 trimethylation in adult differentiated colon associated to cancer DNA hypermethylation. / Rada-Iglesias, Alvaro; Enroth, Stefan; Andersson, Robin; Wanders, Alkwin; Påhlman, Lars; Komorowski, Jan; Wadelius, Claes.
In: Epigenetics : official journal of the DNA Methylation Society, Vol. 4, No. 2, 16.02.2009, p. 107-13.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Histone H3 lysine 27 trimethylation in adult differentiated colon associated to cancer DNA hypermethylation
AU - Rada-Iglesias, Alvaro
AU - Enroth, Stefan
AU - Andersson, Robin
AU - Wanders, Alkwin
AU - Påhlman, Lars
AU - Komorowski, Jan
AU - Wadelius, Claes
PY - 2009/2/16
Y1 - 2009/2/16
N2 - DNA hypermethylation of gene promoters is a common epigenetic alteration occurring in cancer cells. However, little is known about the mechanisms instructing these cancer-specific DNA hypermethylation events. Recent reports have suggested that genes bound by polycomb/Histone H3 lysine 27 trimethylation (H3K27me3) in embryonic stem (ES) cells are frequent targets for cancer-specific DNA hypermethylation. This polycomb-premarking is assumed to be restrained to ES cells, even though almost no polycomb/H3K27me3 binding profiles are available for differentiated tissues. We generated H3K27me3 profiles in human normal colon and they significantly overlapped with those of ES cells and genes hypermethylated in colorectal cancer (CRC). Moreover, colon H3K27me3 was more restricted to genes hypermethylated in CRC, while ES H3K27me3 was also common in genes hypermethylated in other tumors. Therefore, the suggested polycomb pre-marking of genes for cancer DNA hypermethylation is not necessarily limited to ES or early precursor cells but can occur later in differentiated tissues.
AB - DNA hypermethylation of gene promoters is a common epigenetic alteration occurring in cancer cells. However, little is known about the mechanisms instructing these cancer-specific DNA hypermethylation events. Recent reports have suggested that genes bound by polycomb/Histone H3 lysine 27 trimethylation (H3K27me3) in embryonic stem (ES) cells are frequent targets for cancer-specific DNA hypermethylation. This polycomb-premarking is assumed to be restrained to ES cells, even though almost no polycomb/H3K27me3 binding profiles are available for differentiated tissues. We generated H3K27me3 profiles in human normal colon and they significantly overlapped with those of ES cells and genes hypermethylated in colorectal cancer (CRC). Moreover, colon H3K27me3 was more restricted to genes hypermethylated in CRC, while ES H3K27me3 was also common in genes hypermethylated in other tumors. Therefore, the suggested polycomb pre-marking of genes for cancer DNA hypermethylation is not necessarily limited to ES or early precursor cells but can occur later in differentiated tissues.
KW - Adult
KW - Colon
KW - Colonic Neoplasms
KW - DNA Methylation
KW - Embryonic Stem Cells
KW - Histones
KW - Humans
KW - Lysine
KW - Methylation
KW - Polycomb-Group Proteins
KW - Repressor Proteins
M3 - Journal article
C2 - 19276669
VL - 4
SP - 107
EP - 113
JO - Epigenetics
JF - Epigenetics
SN - 1559-2294
IS - 2
ER -
ID: 106775893