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ヒト神経膠芽腫細胞におけるシスプラチン／温熱同時併用処理によるp53依存性HSF活性化抑制：小久保菜穂子¹,松本英樹¹,林　幸子¹,畑下昌範¹,塩浦宏樹²,大坪俊雄³,北井隆平⁴,加納永一¹（福井医大・¹放基,³耳,⁴脳外,²市立泉佐野病院・放）

p53-dependent suppression of heat-induced HSF activation by CDDP in human glioblastoma cells.: Nahoko KOKUBO¹, Hideki MATSUMOTO¹, Sachiko HAYASHI¹, Masanori HATASHITA¹, Hiroki SHIOURA², Toshio OHTSUBO3, Ryuhei KITAI⁴ and Eiichi KANO¹ (¹Depts. of Exptl' Radiol., ³Otorhinolaryngol., ⁴Neurosurg., Fukui Med. Univ., ²Div. Radiol., Izumisano Hosp.)

Purpose: The kinetics of the accumulation of inducible 72-kD heat shock protein (hsp72) and the activation of heat shock transcriptional factor (HSF) after hyperthermia and/or CDDP treatment in two human glioblastoma cell lines, A-172 having the wild-type p53 gene and T98G having the mutated p53 gene were evaluated.
Methods and Materials: Western blot analysis of hsp72, gel-mobility shift assay of HSF, cell survival and development of thermotolerance were examined.
Results: The prominent suppression of heat-induced hsp72 accumulation by CDDP was seen in A-172 cells, but not in T98G cells. This was due to the p53-dependent inhibition of heat-induced HSF activation by CDDP. The interactive hyperthermic enhancement of CDDP cytotoxicity was observed in A-172 cells, but not in T98G cells. In addition, the heat-induced thermotolerance was suppressed by the presence of CDDP in the pre-treatment.
Conclusion: Suppression of heat-induced hsp72 accumulation by CDDP and an interactive thermal chemoenhancement were observed only in the cells bearing the wild-type p53 gene, suggesting enhancement in the cellular thermosensitivity.