PMID- 24939851
OWN - NLM
STAT- MEDLINE
DCOM- 20141215
LR  - 20211124
IS  - 1083-351X (Electronic)
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 289
IP  - 31
DP  - 2014 Aug 1
TI  - Role of activating transcription factor 3 (ATF3) in endoplasmic reticulum (ER) 
      stress-induced sensitization of p53-deficient human colon cancer cells to tumor 
      necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-mediated 
      apoptosis through up-regulation of death receptor 5 (DR5) by zerumbone and 
      celecoxib.
PG  - 21544-61
LID - 10.1074/jbc.M114.558890 [doi]
AB  - Death receptor 5 (DR5) is a death domain-containing transmembrane receptor that 
      triggers cell death upon binding to its ligand, TNF-related apoptosis-inducing 
      ligand (TRAIL), and a combination of TRAIL and agents that increase the 
      expression of DR5 is expected to be a novel anticancer therapy. In this report, 
      we demonstrate that the stress response gene ATF3 is required for endoplasmic 
      reticulum stress-mediated DR5 induction upon zerumbone (ZER) and celecoxib (CCB) 
      in human p53-deficient colorectal cancer cells. Both agents activated PERK-eIF2alpha 
      kinases and induced the expression of activating transcription factor 4 
      (ATF4)-CCAAT enhancer-binding protein (C/EBP) homologous protein, which were 
      remarkably suppressed by reactive oxygen species scavengers. In the absence of 
      ATF3, the induction of DR5 mRNA and protein was abrogated significantly, and this 
      was associated with reduced cell death by cotreatment of TRAIL with ZER or CCB. 
      By contrast, exogenous expression of ATF3 caused a more rapid and elevated 
      expression of DR5, resulting in enhanced sensitivity to apoptotic cell death by 
      TRAIL/ZER or TRAIL/CCB. A reporter assay demonstrated that at least two ATF/cAMP 
      response element motifs as well as C/EBP homologous protein motif at the proximal 
      region of the human DR5 gene promoter were required for ZER-induced DR5 gene 
      transcription. Taken together, our results provide novel insights into the role 
      of ATF3 as an essential transcription factor for p53-independent DR5 induction 
      upon both ZER and CCB treatment, and this may be a useful biomarker for 
      TRAIL-based anticancer therapy.
CI  - (c) 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
FAU - Edagawa, Makoto
AU  - Edagawa M
AD  - From the Department of Biochemical Genetics, Medical Research Institute, Tokyo 
      Medical and Dental University, Tokyo, 113-8510, Japan, the Department of Surgery 
      and Sciences, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 
      812-8582, Japan, and.
FAU - Kawauchi, Junya
AU  - Kawauchi J
AD  - From the Department of Biochemical Genetics, Medical Research Institute, Tokyo 
      Medical and Dental University, Tokyo, 113-8510, Japan.
FAU - Hirata, Manabu
AU  - Hirata M
AD  - From the Department of Biochemical Genetics, Medical Research Institute, Tokyo 
      Medical and Dental University, Tokyo, 113-8510, Japan.
FAU - Goshima, Hiroto
AU  - Goshima H
AD  - From the Department of Biochemical Genetics, Medical Research Institute, Tokyo 
      Medical and Dental University, Tokyo, 113-8510, Japan.
FAU - Inoue, Makoto
AU  - Inoue M
AD  - From the Department of Biochemical Genetics, Medical Research Institute, Tokyo 
      Medical and Dental University, Tokyo, 113-8510, Japan.
FAU - Okamoto, Tatsuro
AU  - Okamoto T
AD  - the Department of Surgery and Sciences, Graduate School of Medical Sciences, 
      Kyushu University, Fukuoka, 812-8582, Japan, and.
FAU - Murakami, Akira
AU  - Murakami A
AD  - the Division of Food Science and Biotechnology, Graduate School of Agriculture, 
      Kyoto University, Kyoto 606-8502, Japan.
FAU - Maehara, Yoshihiko
AU  - Maehara Y
AD  - the Department of Surgery and Sciences, Graduate School of Medical Sciences, 
      Kyushu University, Fukuoka, 812-8582, Japan, and.
FAU - Kitajima, Shigetaka
AU  - Kitajima S
AD  - From the Department of Biochemical Genetics, Medical Research Institute, Tokyo 
      Medical and Dental University, Tokyo, 113-8510, Japan, kita.bgen@mri.tmd.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140617
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (ATF3 protein, human)
RN  - 0 (Activating Transcription Factor 3)
RN  - 0 (DNA Primers)
RN  - 0 (Pyrazoles)
RN  - 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand)
RN  - 0 (Sesquiterpenes)
RN  - 0 (Sulfonamides)
RN  - 0 (TNF-Related Apoptosis-Inducing Ligand)
RN  - 0 (TNFSF10 protein, human)
RN  - 471-05-6 (zerumbone)
RN  - JCX84Q7J1L (Celecoxib)
SB  - IM
MH  - Activating Transcription Factor 3/genetics/*physiology
MH  - Apoptosis/drug effects/*physiology
MH  - Base Sequence
MH  - Celecoxib
MH  - Cell Line, Tumor
MH  - Colonic Neoplasms/*pathology
MH  - DNA Primers
MH  - Endoplasmic Reticulum/*physiology
MH  - Humans
MH  - Promoter Regions, Genetic
MH  - Pyrazoles/pharmacology
MH  - Receptors, TNF-Related Apoptosis-Inducing Ligand/genetics/*metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Sesquiterpenes/pharmacology
MH  - Sulfonamides/pharmacology
MH  - TNF-Related Apoptosis-Inducing Ligand/*physiology
PMC - PMC4118115
OTO - NOTNLM
OT  - ATF3
OT  - Apoptosis
OT  - Cancer Therapy
OT  - Colon Cancer
OT  - DR5
OT  - ER Stress
OT  - Gene Regulation
OT  - Reactive Oxygen Species (ROS)
OT  - p53-independent
EDAT- 2014/06/19 06:00
MHDA- 2014/12/17 06:00
PMCR- 2015/08/01
CRDT- 2014/06/19 06:00
PHST- 2014/06/19 06:00 [entrez]
PHST- 2014/06/19 06:00 [pubmed]
PHST- 2014/12/17 06:00 [medline]
PHST- 2015/08/01 00:00 [pmc-release]
AID - S0021-9258(20)47536-2 [pii]
AID - M114.558890 [pii]
AID - 10.1074/jbc.M114.558890 [doi]
PST - ppublish
SO  - J Biol Chem. 2014 Aug 1;289(31):21544-61. doi: 10.1074/jbc.M114.558890. Epub 2014 
      Jun 17.