Heat-induced drug resistance is associated with increased expression of Bcl-2 in HL60.

HL60 cells underwent apoptosis with heat treatment, i.e. exposure to 42 degrees C for 120 minutes. Cells exposed to the same temperature for 30 minutes became resistant to subsequent, otherwise lethal, heat shock. These thermotolerant cells also acquired resistance to anti-cancer drugs including daunorubicin and VP16. We found that mild heat shock upregulates not only HSP70 but also BCL-2, though BCL-2 has not previously been recognized as a heat-inducible protein. Expression of BCL-2 closely paralleled resistance to subsequent exposure to anticancer drugs. The present results suggest that BCL-2 may play a role in heat-induced drug resistance.