Methylation of Gene CHFR Promoter in Acute Leukemia Cells

In order to explore whether gene CHFR was inactivated by methylation in leukemia cells, the expression of CHFR was examined before and after treatment with demethylation agent in Molt-4, Jurkat and U937 leukemia cell lines by means of RT-PCR, The methylation of promoter in Moh-4, Jurkat and U937 cel...

Full description

Saved in:
Bibliographic Details
Published inJournal of Huazhong University of Science and Technology. Medical sciences Vol. 25; no. 3; pp. 240 - 242
Main Author 龚辉 刘文励 周剑峰 徐慧珍
Format Journal Article
LanguageEnglish
Published China Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China 2005
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:In order to explore whether gene CHFR was inactivated by methylation in leukemia cells, the expression of CHFR was examined before and after treatment with demethylation agent in Molt-4, Jurkat and U937 leukemia cell lines by means of RT-PCR, The methylation of promoter in Moh-4, Jurkat and U937 cells as well as 41 acute leukemia patients was analyzed by MS-PCR. The results showed that methylation of CHFR promoter was inactivated and could be reversed by treatment with a demethylating agent in Molt 4, Jurkat and U937. CHFR promoter methylation was detected in 39 % of acute leukemia patients. There was no difference in incidence of CHFR promoter methylation between acute myeloeytie leukemia and acute lymphocytic leukemia. In conclusion, CHFR is frequently inactivated in acute leukemia and is a good candidate for the leukemia supper gene. By affecting mitotic checkpoint function, CHFR inactivation likely plays a key role in tumorigenesis in acute leukemia. Moreover, the methylation of gene CHFR appears to be a good index with which to predict the sensitivity of acute leukemia to microtubule inhibitors.
Bibliography:42-1679/R
R733.71
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1672-0733
1993-1352
DOI:10.1007/bf02828130