Cisplatin induces the small heat shock protein hsp25 and thermotolerance in Ehrlich ascites tumor cells.

Exposure of Ehrlich ascites tumor (EAT) cells to the anticancer drug cisplatin results in an elevated abundance of three isoforms of the small heat shock protein hsp25 without inducing the general stress response as commonly observed after heat shock. The most effective cisplatin concentration (2.5 microM) is also most efficient in arresting cells in S phase suggesting a relationship between hsp25 expression and cell cycle events. Exposure to cisplatin results also in an increased thermotolerance of EAT cells.