PMID- 31806377
OWN - NLM
STAT- MEDLINE
DCOM- 20200831
LR  - 20200831
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 522
IP  - 4
DP  - 2020 Feb 19
TI  - DR5 related autophagy can promote apoptosis in gliomas after irradiation.
PG  - 910-916
LID - S0006-291X(19)32289-2 [pii]
LID - 10.1016/j.bbrc.2019.11.161 [doi]
AB  - As a cancer treatment strategy, irradiation therapy is widely used that can cause 
      DNA breakage and increase free radicals, which leads to different types of cell 
      death. Among them, apoptosis and autophagy are the most important and the most 
      studied cell death processes. Although the exploration of the relationship 
      between apoptosis and autophagy has been a major area of focus, still the 
      molecular mechanisms of autophagy on apoptosis remain unclear. Here, we have 
      revealed that apoptosis was enhanced by the death receptor 5 (DR5) pathway, and 
      the effect of autophagy on apoptosis was promoted by DR5 interacting with LC3B as 
      well as Caspase8 in gliomas after irradiation. Interestingly, we observed that 
      the addition of four different autophagy inducers, rapamycin (RAP), CCI779, 
      ABT737 and temozolomide (TMZ), induced the differences of DR5 expression and cell 
      apoptosis after irradiation. Unlike RAP and CCI779, ABT737 and TMZ were able to 
      increase DR5 expression and further induce cell death. Therefore, we have 
      concluded that DR5 plays a novel and indispensable role in promoting cell 
      apoptosis under irradiation and suggest a potential therapeutic approach for 
      glioblastoma treatment.
CI  - Copyright (c) 2019 The Authors. Published by Elsevier Inc. All rights reserved.
FAU - Zhang, Peng
AU  - Zhang P
AD  - School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
FAU - Wang, Hailong
AU  - Wang H
AD  - School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
FAU - Chen, Yu
AU  - Chen Y
AD  - School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
FAU - Lodhi, Adil Farooq
AU  - Lodhi AF
AD  - School of Life Science, Beijing Institute of Technology, Beijing, 100081, China; 
      Department of Microbiology, Faculty of Health Sciences, Hazara University, 
      Mansehra, Pakistan.
FAU - Sun, Chunli
AU  - Sun C
AD  - School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
FAU - Sun, Feiyi
AU  - Sun F
AD  - School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
FAU - Yan, Liben
AU  - Yan L
AD  - School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
FAU - Deng, Yulin
AU  - Deng Y
AD  - School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
FAU - Ma, Hong
AU  - Ma H
AD  - School of Life Science, Beijing Institute of Technology, Beijing, 100081, China. 
      Electronic address: 04656@bit.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20191203
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Histones)
RN  - 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand)
RN  - 0 (TNFRSF10B protein, human)
RN  - EC 3.4.22.- (Caspase 8)
SB  - IM
MH  - *Apoptosis/genetics/radiation effects
MH  - *Autophagy/genetics/radiation effects
MH  - Brain Neoplasms/genetics/*pathology/*radiotherapy
MH  - Caspase 8/metabolism
MH  - Cell Line, Tumor
MH  - Gene Expression Regulation, Neoplastic
MH  - Glioma/genetics/*pathology/*radiotherapy
MH  - Histones/metabolism
MH  - Humans
MH  - Methylation
MH  - Receptors, TNF-Related Apoptosis-Inducing Ligand/genetics/*metabolism
MH  - Transcription, Genetic
OTO - NOTNLM
OT  - Apoptosis
OT  - Autophagy
OT  - DR5
OT  - Glioma
OT  - Irradiation tolerance
COIS- Declaration of competing interest None.
EDAT- 2019/12/07 06:00
MHDA- 2020/09/01 06:00
CRDT- 2019/12/07 06:00
PHST- 2019/11/08 00:00 [received]
PHST- 2019/11/24 00:00 [accepted]
PHST- 2019/12/07 06:00 [pubmed]
PHST- 2020/09/01 06:00 [medline]
PHST- 2019/12/07 06:00 [entrez]
AID - S0006-291X(19)32289-2 [pii]
AID - 10.1016/j.bbrc.2019.11.161 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2020 Feb 19;522(4):910-916. doi: 
      10.1016/j.bbrc.2019.11.161. Epub 2019 Dec 3.