Involvement of SAPK/JNK pathway in X-ray-induced rapid cell death of human T-cell leukemia cell line MOLT-4

被引：35

作者：

Enomoto, A

Suzuki, N

Hirano, K

Matsumoto, Y

Morita, A

Sakai, K

Koyama, H

机构：

[1] Univ Tokyo, Grad Sch Med, Dept Radiat Oncol, Bunkyo Ku, Tokyo 1130033, Japan

[2] Cent Res Inst Elect Power Ind, Dept Biosci, Komae Branch, Komae, Tokyo 2018511, Japan

[3] Yokohama City Univ, Kihara Inst, Totsuka Ku, Yokohama, Kanagawa 2440813, Japan

来源：

CANCER LETTERS | 2000年 / 155卷 / 02期

关键词：

X-ray-induced rapid cell death/apoptosis; ceramide; SAPK/JNK; radiation-hybrid;

D O I：

10.1016/S0304-3835(00)00422-5

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

We found that SAPK/JNK was phosphorylated during X-ray-induced rapid cell death of MOLT-4 cells and that acid Sphingomyelinase inhibitor D609 suppressed the rapid cell death as well as phosphorylation of SAPK/JNK. Also C2-ceramide caused phosphorylation of SAPK/JNK, followed by rapid cell death. Further we isolated X-ray-resistant radiation-hybrid clones from MOLT-4 and 50 Gy irradiated mouse FM3A cells by repeated selections with 3 Gy irradiation. One of them named Rh-ia was found resistant to X-ray- as well as C2-ceramide-induced rapid cell death. Rh-1a cells had mouse DNA but no increase in either mouse or human Bcl-2 determined by Western blotting. Accumulation of p53 after X-irradiation was similarly observed in both parental MOLT-4 and Rh-1a cells. However, contrasting to prolonged and prominent phosphorylated status of SAPK/ JNK in MOLT-4 cells, Rh-1a cells exhibited short transient increase and FM3A cells showed no increase of phosphorylated status SAPK/JNK after X-irradiation. Therefore, SAPK/JNK activation is considered important in X-ray-induced rapid cell death or apoptosis of MOLT-4 cells. (C) 2000 Published by Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：137 / 144

页数：8

共 23 条

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