1. Inhibition of HSF1 and SAFB Granule Formation Enhances Apoptosis Induced by Heat Stress.
- Author
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Watanabe K and Ohtsuki T
- Subjects
- Cell Proliferation drug effects, Cell Survival drug effects, Cytoplasmic Granules drug effects, Cytoplasmic Granules metabolism, Gene Knockdown Techniques, Glycols pharmacology, HSP27 Heat-Shock Proteins metabolism, HSP70 Heat-Shock Proteins metabolism, HeLa Cells, Heat Shock Transcription Factors metabolism, Humans, Models, Biological, TRPV Cation Channels antagonists & inhibitors, TRPV Cation Channels metabolism, Temperature, Up-Regulation drug effects, Apoptosis drug effects, Heat Shock Transcription Factors antagonists & inhibitors, Heat-Shock Response drug effects, Matrix Attachment Region Binding Proteins metabolism, Nuclear Matrix-Associated Proteins metabolism, Receptors, Estrogen metabolism
- Abstract
Stress resistance mechanisms include upregulation of heat shock proteins (HSPs) and formation of granules. Stress-induced granules are classified into stress granules and nuclear stress bodies (nSBs). The present study examined the involvement of nSB formation in thermal resistance. We used chemical compounds that inhibit heat shock transcription factor 1 (HSF1) and scaffold attachment factor B (SAFB) granule formation and determined their effect on granule formation and HSP expression in HeLa cells. We found that formation of HSF1 and SAFB granules was inhibited by 2,5-hexanediol. We also found that suppression of HSF1 and SAFB granule formation enhanced heat stress-induced apoptosis. In addition, the upregulation of HSP27 and HSP70 during heat stress recovery was suppressed by 2,5-hexanediol. Our results suggested that the formation of HSF1 and SAFB granules was likely to be involved in the upregulation of HSP27 and HSP70 during heat stress recovery. Thus, the formation of HSF1 and SAFB granules was involved in thermal resistance.
- Published
- 2021
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