간세포암종에서 TPEF의 Methylation에 의한 불활성화
Inactivation of TPEF Gene by Aberrant Methylation in Hepatocellular Carcinoma
정운복, 손윤경, 박지영, 김순영, 전소영, 강구성, 이해암, 김정옥, 김정완,
소속 상세정보
정운복 ( Chung Woon-Bok )
경북대학교 치과대학 구강미생물학교실
손윤경 ( Son Yoon-Kyung )
경북대학교 의과대학 해부병리과학교실
박지영 ( Park Ji-Young )
경북대학교 의과대학 병리학교실
김순영 ( Kim Soon-Young )
경북대학교 치과대학 구강미생물학교실
전소영 ( Chun So-Young )
경북대학교 치과대학 구강미생물학교실
강구성 ( Kang Ku-Seong )
경북대학교 의과대학 병리학교실
이해암 ( Lee Hae-Ahm )
경북대학교 치과대학 구강미생물학교실
김정옥 ( Kim Joung-Ok )
경북대학교 의과대학 병리학교실
김정완 ( Kim Jung-Wan )
경북대학교 치과대학 구강미생물학교실
KMID : 0357920080420010009
Abstract
Background : Abnormalities of genomic methylation patterns have been shown to play a role in the development of carcinoma, and the silencing of tumor suppressor genes is related to local de novo methylation.
Methods : Using methylation specific arbitrarily primed-Polymerase Chain Reaction (Ms AP-PCR), we identified a 322 bp sequence that contained a 5’’un-translated and exon1 regions of the TPEF gene. To evaluate the inactivation of the TPEF gene through hypermethylation in hepatocellular carcinoma (HCC), we investigated the correlation between methylation patterns and TPEF expression in tumor tissues of human HCC and cell lines via a Combined Bisulfite Restriction Assay (CoBRA) and RT-PCR.
Results : A dense methylation pattern of the TPEF was detected in most cell lines, as well as in 10 of the 14 (71.4%) HCC tissues. In addition, loss of heterozygosity (LOH) from the TPEF gene was observed in 5 of the 14 (36%) HCC tissues. Furthermore, RT-PCR analysis revealed TPEF expression in 5 of 8 (62.5%) cell lines. Finally, treatment with a demethylating agent, 5-Aza-2’’deoxycitidine (5-AzaC), increased the expression of TPEF mRNA.
Conclusion : These results indicate that inactivation of the TPEF gene through hypermethylation may be a mechanism by which tumorigenesis occurs in HCC.
키워드
Hypermethylation; HCC; TPEF; CoBRA
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