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前列腺素 E2 通过 DNA 甲基化促进肠道肿瘤生长。

Prostaglandin E2 promotes intestinal tumor growth via DNA methylation.

机构信息

Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

出版信息

Nat Med. 2012 Jan 22;18(2):224-6. doi: 10.1038/nm.2608.

DOI:10.1038/nm.2608
PMID:22270723
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3274627/
Abstract

Although aberrant DNA methylation is considered to be one of the key ways by which tumor-suppressor and DNA-repair genes are silenced during tumor initiation and progression, the mechanisms underlying DNA methylation alterations in cancer remain unclear. Here we show that prostaglandin E(2) (PGE(2)) silences certain tumor-suppressor and DNA-repair genes through DNA methylation to promote tumor growth. These findings uncover a previously unrecognized role for PGE(2) in the promotion of tumor progression.

摘要

虽然异常的 DNA 甲基化被认为是肿瘤抑制基因和 DNA 修复基因在肿瘤发生和发展过程中失活的关键途径之一,但癌症中 DNA 甲基化改变的机制仍不清楚。在这里,我们表明前列腺素 E2(PGE2)通过 DNA 甲基化沉默某些肿瘤抑制基因和 DNA 修复基因,从而促进肿瘤生长。这些发现揭示了 PGE2 在促进肿瘤进展中的一个以前未被认识到的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c530/3274627/4f33dd9c0ce6/nihms338854f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c530/3274627/61e98ee8a24c/nihms338854f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c530/3274627/4f33dd9c0ce6/nihms338854f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c530/3274627/61e98ee8a24c/nihms338854f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c530/3274627/4f33dd9c0ce6/nihms338854f2.jpg

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