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Progesterone receptor gene inactivation and CpG island hypermethylation in human leukemia cancer cells
Author(s) -
Liu Ze-Jun,
Zhang Xiao-Bing,
Zhang Yun,
Yang Xin
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.04.044
Subject(s) - dna methylation , methylation , cancer research , cpg site , biology , leukemia , dnmt1 , microbiology and biotechnology , cancer , gene silencing , gene expression , gene , genetics
Previous studies showed that progesterone receptor (PR), one of the hormone receptor superfamily, was only connected with the sex‐correlated cancers such as breast cancer, endometrial cancer, prostate cancer, etc. This article deals with the PR gene in leukemia. We investigated the methylation status and the expression of the two different PR isoforms, PRA and PRB, in three leukemia cancer cell lines using methylation‐specific polymerase chain reaction (MSP‐PCR) and reverse transcription‐PCR. The correlation of PR methylation and expression together with DNA methyltransferase (DNMT1) was further studied. We found that DNMT1 is required to maintain CpG methylation and aberrant gene silencing of PR gene in human leukemia cancer cells. The activity of 5‐aza‐2 ′ ‐deoxycytidine in demethylation and gene reactivation may be through depleting cellular DNMT1 levels. In addition, extensive methylation of PRA and PRB was also observed in leukemia samples. Our results suggest that PR CpG island aberrant hypermethylation could be one molecular and genetic alteration in leukemia.

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