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The epigenetically‐regulated mi R ‐663 targets H ‐ras in K ‐562 cells
Author(s) -
Yang Yang,
Wang LiLi,
Wang HengXiang,
Guo ZiKuan,
Gao XiaoFang,
Cen Jian,
Li YongHui,
Dou LiPing,
Yu Li
Publication year - 2013
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.12485
Subject(s) - apoptosis , suppressor , cancer research , methylation , cell culture , dna methylation , cell , cell growth , microrna , chemistry , gene , microbiology and biotechnology , biology , gene expression , biochemistry , genetics
miR‐663 is a tumour suppressor that is potentially regulated by modification of C p G islands. Whether aberrant methylation is one of the reasons for miR‐663 down‐regulation in some malignant cells and whether miR‐663 targets oncogenes warrants further research. In the present study, we report that the C p G islands in the upstream region of pre‐miR‐663 are aberrantly methylated in the k‐562 cell line and in the white blood cells of some chronic myelogenous leukaemia patients, and also that H‐ras is one of the genes targeted by miR‐663. Over‐expression of miR‐663 may suppress proliferation of the k‐562 cell line in part by enhancing cell apoptosis.