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Stress response gene ATF3 is a target of c‐ myc in serum‐induced cell proliferation
Author(s) -
Tamura Kiyoshi,
Hua Bayin,
Adachi Susumu,
Guney Isil,
Kawauchi Junya,
Morioka Masaki,
TamamoriAdachi Mimi,
Tanaka Yujiro,
Nakabeppu Yusaku,
Sunamori Makoto,
Sedivy John M,
Kitajima Shigetaka
Publication year - 2005
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7600742
Subject(s) - atf3 , biology , activating transcription factor , gene knockdown , cell growth , transcription factor , ectopic expression , cell cycle , oncogene , gene , creb , gene expression , regulation of gene expression , microbiology and biotechnology , cancer research , promoter , genetics
The c‐ myc proto‐oncogene encodes a transcription factor that promotes cell cycle progression and cell proliferation, and its deficiency results in severely retarded proliferation rates. The ATF3 stress response gene encodes a transcription factor that plays a role in determining cell fate under stress conditions. Its biological significance in the control of cell proliferation and its crosstalk regulation, however, are not well understood. Here, we report that the serum response of the ATF3 gene expression depends on c‐ myc gene and that the c‐Myc complex at ATF/CREB site of the gene promoter plays a role in mediating the serum response. Intriguingly, ectopic expression of ATF3 promotes proliferation of c‐ myc ‐deficient cells, mostly by alleviating the impeded G1‐phase progression observed in these cells, whereas ATF3 knockdown significantly suppresses proliferation of wild‐type cells. Our study demonstrates that ATF3 is downstream of the c‐Myc signaling pathway and plays a role in mediating the cell proliferation function of c‐Myc. Our results provide a novel insight into the functional link of the stress response gene ATF3 and the proto‐oncogene c‐ myc .