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Promoter Hypermethylation of p16 during Neoplastic Transformation of Rat Respiratory Tract Epithelial Cells.

https://repo.qst.go.jp/records/61551
https://repo.qst.go.jp/records/61551
302165ae-e922-4baf-98e6-b5e13c95f528
Item type 会議発表用資料 / Presentation(1)
公開日 2006-06-30
タイトル
タイトル Promoter Hypermethylation of p16 during Neoplastic Transformation of Rat Respiratory Tract Epithelial Cells.
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_c94f
資源タイプ conference object
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Yamada, Yutaka

× Yamada, Yutaka

WEKO 609051

Yamada, Yutaka

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Nakata, Akifumi

× Nakata, Akifumi

WEKO 609052

Nakata, Akifumi

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Shimada, Yoshiya

× Shimada, Yoshiya

WEKO 609053

Shimada, Yoshiya

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山田 裕

× 山田 裕

WEKO 609054

en 山田 裕

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中田 章史

× 中田 章史

WEKO 609055

en 中田 章史

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島田 義也

× 島田 義也

WEKO 609056

en 島田 義也

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内容記述タイプ Abstract
内容記述 To investigate whether p16 hypermethylation is involved in the silencing of p16 expression and the development of rat lung tumors, p16 status and neoplastic transformation of several respiratory tract epithelial cell lines were examined. Analysis utilizing methylation specific PCR (MSP) method revealed that virus-immortalized SV40T2 cells had unmethylated status and that benzo [a] pyrene-induced BP cells displayed heterogeneous methylation status of the p16 promoter region. On the other hand, BP130, BP270 and BP(P)Tu cells derived from BP cells, and gamma ray-transformed RTiv3 cells displayed complete methylation of the gene. The MSP and PCR of genomic DNA in the p16 region did not amplify product in PuD2 cells established from the plutonium-induced lung tumor. Expression analysis of p16 mRNA by RT-PCR demonstrated that SV40T2 and BP cells expressed the p16 transcript. Demethylating agent, 5AzaC demethylated partially the p16 promoter region of BP(P)Tu and BP cells and increased expression of the p16 transcript. Tumorigenicity assay utilizing inoculation of the cells into nude mouse revealed that SV40T2 and RTiv3 cells had no tumorigenicity. Treatment of BP(P)Tu and BP cells with 5AzaC decreased the cell growth in nude mouse. These results indicate that the hypermethylation of p16 promoter region occurs at the early stage of neoplastic transformation processes and the gene silencing following the methylation is partially concerned with the tumorigenicity of rat respiratory tract cells. Homozygous deletion and lack of expression of the p16 may also account for the mechanisms of tumorigenicity.
会議概要(会議名, 開催地, 会期, 主催者等)
内容記述タイプ Other
内容記述 The 6th Japan-France Workshop on Radiobiology and Isotopic Imaging
発表年月日
日付 2006-06-22
日付タイプ Issued
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