Papers - SUZUKI Hiromu

p53によるビタミンD受容体の発現誘導と癌治療への応用

丸山 玲緒, 豊田 実, 青木 文夫, 佐々木 泰史, 明石 浩史, 見田 裕章, 鈴木 拓, 時野 隆至, 今井 浩三, 篠村 恭久

日本臨床分子医学会学術総会プログラム・抄録集 ( 日本臨床分子医学会 )  42回   112 - 112  2005.07

Aberrant methylation and silencing of the BNIP3 gene in colorectal and gastric cancer

M Murai, M Toyota, H Suzuki, A Satoh, Y Sasaki, K Akino, M Ueno, F Takahashi, M Kusano, H Mita, K Yanagihara, T Endo, Y Hinoda, T Tokino, K Imai

CLINICAL CANCER RESEARCH ( AMER ASSOC CANCER RESEARCH )  11 ( 3 ) 1021 - 1027  2005.02  [Refereed]

　View Summary

BNIP3 protein is a proapoptotic member of the Bcl-2 family that is expressed in hypoxic regions of tumors. To examine its role in the progression of gastrointestinal cancer, we examined the expression and DNA methylation status of BNIP3 gene in a panel of colorectal and gastric cancer cell lines. BNIP3 was not expressed in 14 of the 24 cell lines tested, and its absence was not caused by gene mutation or by altered expression of hypoxia inducible factor-1, a key transcription factor that regulates BNIP3 expression. On the other hand, methylation of the 5' CpG island of BNIP3 was closely correlated with silencing the gene. Moreover, treating methylated cells with the methyltransferase inhibitor 5-aza2'-deoxycytidine restored hypoxia-induced expression of BNIP3 mRNA and protein, which in turn led to cell death. Aberrant methylation of BNIP3 was also detected in 66% of primary colorectal and 49% of primary gastric cancers, but not in normal tissue samples collected from areas adjacent to the tumors. Apparently, epigenetic alteration of BNIP3 is a frequent and cancer-specific event, which suggests that inactivation of BNIP3 likely plays a key role in the progression of some gastrointestinal cancers and that it may be a useful molecular target for therapy.

PubMed

Epigenetic inactivation of SFRP's complements genetic alterations to allow constitutive Wnt pathway signaling in human colorectal cancer

S. H., T. M., T. T., M. M., I. K.

Japan Journal of Molecular Tumor Marker Research ( Japanese Society for Molecular Tumor Marker Research )  20   73 - 74  2005

DOI CiNii

【消化器疾患における転写制御メカニズムを解明する】 消化器癌とエピジェネティクスの新たな展開

鈴木拓, 公衆衛生学講座, 野島正寛, 森満, 今井浩三

分子消化器病   1   327 - 335  2004  [Refereed]