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It has been suggested that inducible heat shock proteins(HSPsmay function in multiple roles in cytoprotection. Howeverrecent reports have shown that nitric oxide(NOradicals are an initiator of heat‑and radio‑resistanceand act through the activation of the human homolog of MDM2(HDM2 the depression of p53 accumulationand the induction of NO synthase(iNOSor alternativelyNOS2 which is observed following a priming irradiation. The aim of this work was to acquire additional information on the roles of p53HDM2iNOSNO radicalsand HSPs on the development of heat‑and radio‑resistance as following a priming heat treatment. Wild‑type(wtp53 and mutated (mp53 cells were used. These cells were derived from the H1299 human lung cancer cell line in which p53 is deleted. Cellular sensitivities were determined with a colony‑forming assay. In both pre‑heated wtp53 cells and in pre‑heated mp53 cellsthe induction of heat‑and radio‑resistance was observed in the absence of KNK437(an inhibitor of HSPsand in the presence of RITA (an inhibitor of p53‑HDM2 interactions aminoguanidine(an iNOS inhibitoror c‑PTIO(an NO radical scavenger. These findings suggest that following a priming heat treatmentHSPs contribute to heat‑and radio‑resistance.

A Priming Heat Treatment Can Induce the Development of Heat- and Radio-resistance via HSPs, Regardless of p53-gene Status