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.
Highlights
Eukaryotic cells possess stress response mechanisms that are induced by environmental stresses, including heat, radiation, and chemical reagents [1,2]
These findings indicated that heat shock transcription factor 1 (HSF1) and scaffold attachment factor B (SAFB) were involved in thermal resistance
These 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, causing enhanced cell growth inhibition
Summary
Eukaryotic cells possess stress response mechanisms that are induced by environmental stresses, including heat, radiation, and chemical reagents [1,2]. The major stress resistance mechanisms include translational arrest, upregulation of heat shock proteins (HSPs), and formation of granules [3,4,5,6]. LLPS is mediated by multivalent weak interactions conferred by a low complexity sequence domain of RNA-binding proteins. NSBs are transiently formed due to heat stress and disappear during the recovery period [5]. These reports suggest the involvement of nSBs in thermal resistance. The present study investigated the involvement of nSB formation in thermal resistance by determining the effect of inhibitor compounds on granule formation and HSP expression in vitro
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