PMID- 24530917
OWN - NLM
STAT- MEDLINE
DCOM- 20140603
LR  - 20161125
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 445
IP  - 2
DP  - 2014 Mar 7
TI  - Role of ATF3 in synergistic cancer cell killing by a combination of HDAC 
      inhibitors and agonistic anti-DR5 antibody through ER stress in human colon 
      cancer cells.
PG  - 320-6
LID - S0006-291X(14)00228-9 [pii]
LID - 10.1016/j.bbrc.2014.01.184 [doi]
AB  - Histone deacetylase inhibitors (HDACIs) are promising agents for cancer therapy. 
      However, the mechanism(s) responsible for the efficacy of HDACIs have not yet to 
      be fully elucidated. Death receptor 5 (DR5) is a transmembrane receptor 
      containing death domain that triggers cell death upon binding to TRAIL (tumor 
      necrosis factor-related apoptosis-inducing ligand) or agonistic anti-DR5 
      monoclonal antibody, and the combination of TRAIL/agonistic anti-DR5 monoclonal 
      antibody and agents that increase the expression of DR5 is expected as a novel 
      anticancer therapeutic strategy. Here we report that six different HDACIs 
      activated endoplasmic reticulum (ER) stress sensor PERK and eIF2alpha and induced the 
      ATF4/ATF3/CHOP pathway in p53-deficient human colon cancer cells. This resulted 
      in an increased expression of DR5 on the cell surface and sensitized cells to 
      apoptosis by agonistic anti-DR5 monoclonal antibody. Stress response gene ATF3 
      was required for efficient DR5 induction by HDACIs, and DR5 reporter assay showed 
      that ATF3 play crucial role for the HDACIs-induced activation of DR5 gene 
      transcription. These provide important mechanistic insight into how HDACIs 
      exhibit pro-apoptotic activity in clinical anti-cancer treatments when they are 
      used in combination with other therapeutic strategies.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Liu, Jia
AU  - Liu J
AD  - Department of Biochemical Genetics, Medical Research Institute, Tokyo Medical and 
      Dental University, Tokyo 113-8510, Japan; Department of Immunology, Norman 
      Bethune College of Medicine, Jilin University, Changchun, Jilin 130021, China; 
      Department of Thyroid Surgery, First Hospital of Jilin University, Changchun, 
      Jilin 130021, China.
FAU - Edagawa, Makoto
AU  - Edagawa M
AD  - Department of Biochemical Genetics, Medical Research Institute, Tokyo Medical and 
      Dental University, Tokyo 113-8510, Japan.
FAU - Goshima, Hiroto
AU  - Goshima H
AD  - Department of Biochemical Genetics, Medical Research Institute, Tokyo Medical and 
      Dental University, Tokyo 113-8510, Japan.
FAU - Inoue, Makoto
AU  - Inoue M
AD  - Department of Biochemical Genetics, Medical Research Institute, Tokyo Medical and 
      Dental University, Tokyo 113-8510, Japan.
FAU - Yagita, Hideo
AU  - Yagita H
AD  - Department of Immunology, Juntendo University School of Medicine, Tokyo 113-8421, 
      Japan.
FAU - Liu, Zhonghui
AU  - Liu Z
AD  - Department of Immunology, Norman Bethune College of Medicine, Jilin University, 
      Changchun, Jilin 130021, China. Electronic address: liuzh@jlu.edu.cn.
FAU - Kitajima, Shigetaka
AU  - Kitajima S
AD  - Department of Biochemical Genetics, Medical Research Institute, Tokyo Medical and 
      Dental University, Tokyo 113-8510, Japan. Electronic address: 
      kita.bgen@mri.tmd.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140212
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (ATF3 protein, human)
RN  - 0 (Activating Transcription Factor 3)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (DDIT3 protein, human)
RN  - 0 (Histone Deacetylase Inhibitors)
RN  - 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 147336-12-7 (Transcription Factor CHOP)
RN  - EC 2.7.11.1 (EIF2AK3 protein, human)
RN  - EC 2.7.11.1 (eIF-2 Kinase)
SB  - IM
MH  - Activating Transcription Factor 3/genetics/*metabolism
MH  - Antibodies, Monoclonal/immunology/*pharmacology
MH  - Apoptosis
MH  - Cell Line, Tumor
MH  - Colon/drug effects/metabolism/pathology
MH  - Colonic Neoplasms/*drug therapy/genetics/metabolism/pathology
MH  - Drug Synergism
MH  - Endoplasmic Reticulum Stress/*drug effects
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Gene Knockdown Techniques
MH  - Histone Deacetylase Inhibitors/chemistry/*pharmacology
MH  - Humans
MH  - Receptors, TNF-Related Apoptosis-Inducing Ligand/*genetics/immunology
MH  - Signal Transduction/drug effects
MH  - Transcription Factor CHOP/genetics/metabolism
MH  - Tumor Suppressor Protein p53/genetics
MH  - Up-Regulation/drug effects
MH  - eIF-2 Kinase/metabolism
OTO - NOTNLM
OT  - ATF3
OT  - Agonistic anti-DR5 antibody
OT  - DR5
OT  - ER stress
OT  - HDACI
EDAT- 2014/02/18 06:00
MHDA- 2014/06/04 06:00
CRDT- 2014/02/18 06:00
PHST- 2014/01/28 00:00 [received]
PHST- 2014/01/29 00:00 [accepted]
PHST- 2014/02/18 06:00 [entrez]
PHST- 2014/02/18 06:00 [pubmed]
PHST- 2014/06/04 06:00 [medline]
AID - S0006-291X(14)00228-9 [pii]
AID - 10.1016/j.bbrc.2014.01.184 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2014 Mar 7;445(2):320-6. doi: 
      10.1016/j.bbrc.2014.01.184. Epub 2014 Feb 12.