RRC ID 75058
著者 Watanabe K, Ohtsuki T.
タイトル Inhibition of HSF1 and SAFB Granule Formation Enhances Apoptosis Induced by Heat Stress.
ジャーナル Int J Mol Sci
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.
巻・号 22(9)
公開日 2021-5-7
DOI 10.3390/ijms22094982
PII ijms22094982
PMID 34067147
PMC PMC8124827
MeSH Apoptosis* / drug effects 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 / antagonists & inhibitors* Heat Shock Transcription Factors / metabolism Heat-Shock Response* / drug effects Humans Matrix Attachment Region Binding Proteins / metabolism* Models, Biological Nuclear Matrix-Associated Proteins / metabolism* Receptors, Estrogen / metabolism* TRPV Cation Channels / antagonists & inhibitors TRPV Cation Channels / metabolism Temperature Up-Regulation / drug effects
IF 4.556
リソース情報
ヒト・動物細胞 HeLa