Association between overexpression of heat shock protein (HSP27) and anticancer agents with different cytotoxic mechanisms in BG-1 ovarian cancer cells and HeLa cervical cancer cells *
Purpose:To determine the factors associated with overexpression of HSP27 in two gynecologic cell lines when treated with anticancer drugs which induce the G2/M block with different cytotoxic mechanisms. Method:BG-1 ovarian cancer cells and HeLa cervical cancer cells were treated with a topoisomerase Ⅱ inhibitor (etoposide). tubulin polymerization inhibitors(colcemid and vincristine), a tubulin depolymerization inhibitor(paclitaxel) or a membrane-associated anticancer drug(ＥＴ-18-ＯＣＨ3). Growth arrest of the cells was evaluated by counting cell numbers. Propidium iodide staining and flow cytometrie analysis were applied for determination of cell cycle perturbation. HSP27 was stained by the indirect immunofluorescence technique and analyzed by a flow cytometer. Result:Growth arrest and G2/M accumulation were dependent on the dose of each cytotoxic agent. There were positive correlations between HSP27 overexpression and G2/M accumulation when BG-1 cells were treated with etoposide. colcemid. vincristine. and ET-18-OCH3 but not with paclitaxel. Similar results were seen with HeLa cells but ET-18-OCH3 treatment did not induce overexpression of HSP27. Conclusion:Overexpression of HSP27 was associated with etoposide, colcemid, and vincristine treatment. There was no correlation between paclitaxel treatment and HSP overexpression. Expression of HSP27 by ET-18-OCH3 was cell dependent. (Accepted on September 14, 2000) Kawasaki Igakkaishi 26 (4) : 203-210. 2000
