PMID- 31863666
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220412
IS  - 2228-5806 (Print)
IS  - 2228-5814 (Electronic)
IS  - 2228-5806 (Linking)
VI  - 22
IP  - 3
DP  - 2020 Oct
TI  - Endoplasmic Reticulum Stress Induces miR-706, A Pro-Cell Death microRNA, in A 
      Protein Kinase RNA-Like ER Kinase (PERK) and Activating Transcription Factor 4 
      (ATF4) Dependent Manner.
PG  - 394-400
LID - 10.22074/cellj.2020.6873 [doi]
AB  - OBJECTIVE: Endoplasmic reticulum (ER) stress causes an adaptive response 
      initiated by protein kinase RNA-like ER kinase (PERK), Ire1 and ATF6. It has been 
      reported that these upstream regulators induce microRNAs. The current study was 
      designed to find a novel microRNA that mediates ER stress components and finally 
      contributes to cell fate decision. MATERIALS AND METHODS: In this experimental 
      study, miR-706 levels were checked under different conditions of ER stress 
      induced by Thapsigargin, Tunicamycin or low glucose media. PERK and ATF4 were 
      knocked-down by administration of lentivirus-mediated short hairpin RNA to 
      explore the effect of ER stress related proteins on miR-706 expression. The 
      effect of miR-706 on caspase activity and apoptosis inhibitor 1 (CAAP1) levels 
      were examined by using mimic-miR-706. The role of CAAP1 in inhibiting cell death 
      (measured by Annexin V staining) and contributing to patient overall survival 
      (measured by Kaplan-Meier estimate) were further confirmed by antimiR- 706 and 
      CAAP1 knock-down. RESULTS: We showed that Thapsigargin or Tunicamycin triggered 
      ER stress leading to the induction of miR-706. miR-706 induction is dependent on 
      PERK and its downstream regulator ATF4, as knocking-down of PERK and ATF4 
      suppressed miR-706 induction in response to ER stress. Knocking-down of miR-706 
      reduces cell death triggered by ER stress, indicating that miR-706 is pro-cell 
      death microRNA. We further identified CAAP1 as a miR-706 target in regulating ER 
      stress initiated cell death. CONCLUSION: Collectively, our results pointed to an 
      ER signaling network consisting of proteins, microRNA and novel target.
CI  - Copyright(c) by Royan Institute. All rights reserved.
FAU - Wang, Xiu
AU  - Wang X
AD  - Department of Anesthesiology, The Fourth Affiliated Hospital of China Medical 
      University, Shenyang, Liaoning, China. Electronic Address: a6860330@yahoo.com.
FAU - Han, Yi
AU  - Han Y
AD  - The Second Department of Urology, Shenyang Red Cross Hospital, Shenyang, People's 
      Republic of China (CHN).
FAU - Hu, Guodong
AU  - Hu G
AD  - The Second Department of Urology, Shenyang Red Cross Hospital, Shenyang, People's 
      Republic of China (CHN).
FAU - Guo, Jianbo
AU  - Guo J
AD  - The Third Department of General Surgery, The Fourth affiliated Hospital of China, 
      Medical University, Shenyang, Liaoning, China.
FAU - Chen, Hongyu
AU  - Chen H
AD  - The Second Department of Urology, Shenyang Red Cross Hospital, Shenyang, People's 
      Republic of China (CHN).
LA  - eng
PT  - Journal Article
DEP - 20191215
PL  - Iran
TA  - Cell J
JT  - Cell journal
JID - 101566618
PMC - PMC6947010
OTO - NOTNLM
OT  - Activating Transcription Factor 4
OT  - Caspase Activity and Apoptosis Inhibitor 1
OT  - Endoplasmic Reticulum Stress
OT  - Protein Kinase RNA-Like ER Kinase
OT  - miR-706
COIS- There is no conflict of interest in this study.
EDAT- 2019/12/22 06:00
MHDA- 2019/12/22 06:01
PMCR- 2020/10/01
CRDT- 2019/12/22 06:00
PHST- 2019/01/01 00:00 [received]
PHST- 2019/06/22 00:00 [accepted]
PHST- 2019/12/22 06:00 [entrez]
PHST- 2019/12/22 06:00 [pubmed]
PHST- 2019/12/22 06:01 [medline]
PHST- 2020/10/01 00:00 [pmc-release]
AID - 10.22074/cellj.2020.6873 [doi]
PST - ppublish
SO  - Cell J. 2020 Oct;22(3):394-400. doi: 10.22074/cellj.2020.6873. Epub 2019 Dec 15.