Heat shock-mediated cell cycle arrest is accompanied by induction of p21 CKI.

Heat shock induces several events in cells including a series of gene expressions and cell cycle arrest. Recently, several types of cell cycle arrest have been related to the function of cyclin-dependent kinase inhibitors (CKI). Here we show that heat shock treatment up-regulates p21 CKI mRNA and protein in A172 glioma cells and arrests the cell cycle at the G1 phase, p53-deficient cell lines, MDAH041 and T98G, also showed a significant increase in p21 CKI expression after heat stress, indicating that the induction involves a p53-independent pathway. The kinetics of this transient induction, which is not affected by cycloheximide, demonstrate that p21 CKI is an immediate-early response gene.