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Role of activating transcription factor 3 protein ATF 3 in necrosis and apoptosis induced by 5‐fluoro‐2′‐deoxyuridine
Author(s) -
Sato Akira,
Nakama Kentaro,
Watanabe Hiroki,
Satake Akito,
Yamamoto Akihiro,
Omi Takuya,
Hiramoto Akiko,
Masutani Mitsuko,
Wataya Yusuke,
Kim HyeSook
Publication year - 2014
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.12752
Subject(s) - apoptosis , necrosis , gene knockdown , programmed cell death , tumor necrosis factor alpha , hsp27 , microbiology and biotechnology , heat shock protein , uvb induced apoptosis , chemistry , biology , cancer research , immunology , hsp70 , caspase , biochemistry , genetics , gene
Necrosis and apoptosis are the two major forms of cell death. We have studied the mechanisms that regulate the cell death observed during treatment of mouse cancer cell line FM 3A with the anticancer drug 5‐fluoro‐2′‐deoxyuridine ( FU dR). To detect causal differences between necrosis and apoptosis, we exploited the necrosis in original clone F28‐7 and the apoptosis in its variant F28‐7‐A that occur on treatment with FU dR. Activating transcription factor 3 ( ATF 3) was strongly induced during necrosis but not apoptosis. In addition, we found that ATF 3 expression is regulated by heat shock protein 90 ( HS P90) at the m RNA stage. Knockdown of Atf3 by si RNA in the F28‐7 cells resulted in apoptotic morphology rather than necrotic morphology. These results suggest that ATF 3 is a cell‐death regulator in necrosis and apoptosis.