Identification of differentially methylated CpG islands in prostate cancer

International Journal of Cancer. Journal International Du Cancer
Yasushi YamadaMasatoshi Watanabe

Abstract

Epigenetic change such as DNA methylation is one important mechanism for regulating gene expression as genetic change, such as mutation or loss of heterozygosity. Methylation of cancer-related genes has been shown to play an important role in carcinogenesis and tumor progression. Using methylated CpG island amplification (MCA)/representational difference analysis (RDA), we identified four CpG islands in neurotrophin tyrosine kinase receptor type 2 (NTRK2), Protocadherine Flamingo1 and MFPC (Methylated Fragments in Prostate Cancer) 7 and 8. Bisulfite sequencing revealed that 2 regions of NTRK2 as well as MFPC7 and MFPC8 were aberrantly methylated in prostate cancer cell lines, and COBRA showed that 48 (76.24%), 37 (58.7%) and 14 (22.2%) of 63 prostate cancer tissues were methylated, respectively, for these sites. On the other hand, none of 13 benign prostate samples were methylated, except for 1 (7.7%) with NTRK2. For NTRK2, mRNA expression was negative in prostate cancer cell lines (LNCaP and DU145) but was recovered on a methyltransferase inhibitor (5-Aza-CdR) treatment. The role of NTRK2 within NTRK remains unclear. Our results suggest that these 3 hypermethylated DNA fragments also may be markers of prostate cancer detection.

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Citations

Mar 26, 2004·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Katsuhiko TerasawaRyuichi Kudo
Jan 8, 2010·Molecular Cancer Therapeutics·Dhruva Kumar MishraJaydutt V Vadgama
Feb 16, 2006·British Journal of Cancer·K TerasawaT Tokino
Dec 15, 2005·International Journal of Cancer. Journal International Du Cancer·Xiaolei FangDawei Xu
Feb 18, 2021·Journal of Translational Medicine·Zijian ChenHuichuan Yu

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