| Literature DB >> 26883180 |
Nobuhisa Yamada1, Kohichiroh Yasui1, Osamu Dohi1, Yasuyuki Gen1, Akira Tomie1, Tomoko Kitaichi1, Naoto Iwai1, Hironori Mitsuyoshi1, Yoshio Sumida1, Michihisa Moriguchi1, Kanji Yamaguchi1, Taichiro Nishikawa1, Atsushi Umemura1, Yuji Naito1, Shinji Tanaka2, Shigeki Arii2, Yoshito Itoh1.
Abstract
Epigenetic changes as well as genetic changes are mechanisms of tumorigenesis. We aimed to identify novel genes that are silenced by DNA hypermethylation in hepatocellular carcinoma (HCC). We screened for genes with promoter DNA hypermethylation using a genome-wide methylation microarray analysis in primary HCC (the discovery set). The microarray analysis revealed that there were 2,670 CpG sites that significantly differed in regards to the methylation level between the tumor and non-tumor liver tissues; 875 were significantly hypermethylated and 1,795 were significantly hypomethylated in the HCC tumors compared to the non‑tumor tissues. Further analyses using methylation-specific PCR, combined with expression analysis, in the validation set of primary HCC showed that, in addition to three known tumor-suppressor genes (APC, CDKN2A, and GSTP1), eight genes (AKR1B1, GRASP, MAP9, NXPE3, RSPH9, SPINT2, STEAP4, and ZNF154) were significantly hypermethylated and downregulated in the HCC tumors compared to the non-tumor liver tissues. Our results suggest that epigenetic silencing of these genes may be associated with HCC.Entities:
Mesh：
Year: 2016 PMID： 26883180 DOI： 10.3892/or.2016.4619
Source DB: PubMed Journal: Oncol Rep ISSN： 1021-335X Impact factor: 3.906