Epigenetic inactivation of class II transactivator (CIITA) is associated with the absence of interferon-γ-induced HLA-DR expression in colorectal and gastric ... View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2004-10-04

AUTHORS

Ayumi Satoh, Minoru Toyota, Hideyuki Ikeda, Yoshikazu Morimoto, Kimishige Akino, Hiroaki Mita, Hiromu Suzuki, Yasushi Sasaki, Takayuki Kanaseki, Yukio Takamura, Hidenobu Soejima, Takeshi Urano, Kazuyoshi Yanagihara, Takao Endo, Yuji Hinoda, Masahiro Fujita, Masao Hosokawa, Noriyuki Sato, Takashi Tokino, Kohzoh Imai

ABSTRACT

Tightly regulated at the level of transcription, expression of MHC class II molecules varies significantly among gastrointestinal cancers. High levels of MHC class II expression are often associated with a better prognosis, which is indicative of the involvement of CD4+ lymphocytes in tumor suppression, but the molecular mechanism by which MHC class II expression is regulated remains unclear. In the present study, we investigated the expression of one inducible MHC class II molecule, HLA-DR, and its coactivators in a panel of colorectal and gastric cancer cell lines. Interferon-γ induced expression of HLA-DR in 14 of 20 cell lines tested; the remaining six cell lines did not express HLA-DR. Analysis of the expression of transcription factors and coactivators associated with HLA-DR revealed that the loss of CIITA expression was closely associated with the absence of HLA-DR induction. Moreover, DNA methylation of the 5′ CpG island of CIITA-PIV was detected in all cancer cells that lacked CIITA. The methylation and resultant silencing of CIITA-PIV depended on the activities of two DNA methyltransferases, DNMT1 and DNMT3B, and their genetic inactivation restored CIITA-PIV expression. It thus appears that CIITA methylation is a key mechanism that enables some gastrointestinal cancer cells to escape immune surveillance. More... »

PAGES

8876-8886

Journal

TITLE

Oncogene

ISSUE

55

VOLUME

23

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1208144

DOI

http://dx.doi.org/10.1038/sj.onc.1208144

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1010763904

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/15467734


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