Analysis of thermotolerance mechanism in carcinoma thermotherapy by cDNA microarrays method

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In carcinoma hyperthermia therapy, we have experienced carcinoma to be cured well and the carcinoma that are not cured. It is thought that there is a difference of thermosensibility and thermotolerance of cancer cell, but an essential factor is not yet clarified. We analyze thermosensibility, thermotolerance mechanism with cDNA microarrays method and an confirmed inductive gene. We demanded relation with thermosensibility, thermotolerance and DNA double strand breaks with lung fibroblast scid cells suffered a loss in DNA double strand breaks repair and Hybrid scid cells. A Scid cell is radiosensitive, and the Hybrid Scid cell which introduced the human chromosome8 into recovers to normal radiosensitive. We examined an effect of thermotolerance inhibitor Vitamin K2. Scid cells showed high thermosensibility in comparison with Hybrid Scid cells and a Balb/c 3T3 cells using control. We observed intranuclear Y-H2AX focus after hyperthermia processed a Scid cell. We gradually decreased with a maximum after hyperthermia disposal afterwards in 30 minutes. The Y-H2AX focus increased with hyperthermia treatment time. There was different clearly when it compared the number of the Y-H2AX focus of a Scid cells with Hybrid Scid cells and Balb/c 3T3 cells. A correlation was seen in increase and hyperthermia sensibility of intranuclear Y-H2AX focus. Here, we show that vitamin k2 inhibited the expression of heat-shock protein 72 but did not affect the constitutive expression of heat-shock protein 70. VitaminK2 sensitized A549 cells and HaLa cells to heat-treatment induced cell death. These finding suggest that thermosensitivity and thermotolerance of cells might be associated with DNA double-strand break formation.