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Depletion of PDCD4 Accelerates Stress Granule Assembly Through Sensitization of Stress Response Pathways

초록

영어

Programmed cell death 4 (PDCD4) is a novel tumor suppressor that function in the nucleus and the cytoplasm and appears to be involved in the regulation of transcription and translation. Stress granules (SGs) are cytoplasmic foci at which untranslated mRNAs accumulate when cells exposed to environmental stresses. Since PDCD4 has implicated in translation repression through direct interaction with eukaryotic translation initiation factor 4A (eIF4A), we here investigated if PDCD4 has a functional role in the process of SG assembly under oxidative stresses. Using immunofluorescence microscopy, we found that PDCD4 is localized to SGs under oxidative stresses. Next, we tested if knockdown of PDCD4 has an effect on the assembly of SG using PDCD4-specific siRNA. Interestingly, SG assembly was accelerated and this effect was caused by sensitization of phosphorylation of eIF2 and dephosphorylation of eIF4E binding protein (4E-BP). These results suggest that PDCD4 has an effect on SG dynamics and possibly involved in capdependent translation repression under stress conditions.

목차

Abstract
1. Introduction
2. Materials and Methods
2.1 Cell Culture, Transfection and Western Blot Analysis
2.2 Reagents and Antibodies
2.3 RNA Interference
2.4 Immunocytochemistry
3. Results & Discussion
4. Conclusion
Acknowledgement
References

저자정보

  • Jeeho Kim Department of Cellular & Molecular Medicine, College of Medicine, Chosun University, Laboratory of Genomic Instability and Cancer Therapeutics, Cancer Mutation Research Center, College of Medicine, Chosun University
  • In Youb Chang Department of Anatomy, College of Medicine, Chosun University, Gwangju 61452 Republic of Korea
  • Wooje Lee Department of Cellular & Molecular Medicine, College of Medicine, Chosun University, Laboratory of Genomic Instability and Cancer Therapeutics, Cancer Mutation Research Center, College of Medicine, Chosun University
  • Takbum Ohn Department of Cellular & Molecular Medicine, College of Medicine, Chosun University, Laboratory of Genomic Instability and Cancer Therapeutics, Cancer Mutation Research Center, College of Medicine, Chosun University

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