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

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Wang Xiu; HAN YI; Hu Guodong; Guo Jianbo; Chen Hongyu

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Journal: Cell Journal (Yakhteh) Year:2020 | Volume:22 | Issue:3 Page(s): 394-400

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Title

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

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Keywords

Activating Transcription Factor 4

Caspase Activity and Apoptosis Inhibitor 1

Endoplasmic Reticulum Stress

miR-706

Protein Kinase RNA-Like ER Kinase

Abstract

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.

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APA: Copy

Wang, Xiu, HAN, YI, Hu, Guodong, Guo, Jianbo, & Chen, Hongyu. (2020). 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. CELL JOURNAL (YAKHTEH), 22(3), 394-400. SID. https://sid.ir/paper/737831/en

Vancouver: Copy

Wang Xiu, HAN YI, Hu Guodong, Guo Jianbo, Chen Hongyu. 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. CELL JOURNAL (YAKHTEH)[Internet]. 2020;22(3):394-400. Available from: https://sid.ir/paper/737831/en

IEEE: Copy

Xiu Wang, YI HAN, Guodong Hu, Jianbo Guo, and Hongyu Chen, “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,” CELL JOURNAL (YAKHTEH), vol. 22, no. 3, pp. 394–400, 2020, [Online]. Available: https://sid.ir/paper/737831/en

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