グリオーマ細胞を用いてX線、粒子線での染色体異常解析を解析した。放射線増感効果が期待できるNBS1遺伝子の阻害剤であるmirinでCD133+, CD133-細胞で比較を行った。CD133＋のstem like cellはCD133-細胞と比較するとAKTの活性化が促進されることがわかった。DNA損傷を修復する能力がCD133＋のstem like cellは高いことが示唆された。また、正常線維芽細胞の静止期細胞に粒子線およびX線を照射しPLDRに関しても検討を行った。エックス線とことなり粒子線では非対数増殖期でも誤修復が多くPLDRが欠損する原因と考えられ粒子線治療の有効性が示唆された。
We have demonstrated whether AKT is important molecular targets to control the radioresistance through the activation of phospholitated AKT compared between CD133+ and CD133- glioma tumour cells after ionizing radiation treatment. We showed IR-induced AKT phosphorylation in CD133+ tumour cells than CD133- tumour cells when mirin was used. Our data suggested that the tumour cells expressing CD133+, a maker for the stem cell, was induced the activation of AKT more than CD133- cells after radiation. From this result, it may be said that CD133+cells have greater repair activation in response to DNA damage in cellular radiosensitivity. Confluent normal cells were exposed to X-rays and heavy ions and PLDR was studied using FISH technique. It was found that heavy ions induce similar exchanges between PLDR and PLD condition, suggesting that heavy ion therapy is as effective to non-cycling cells as cycling cells.

研究種目 : 基盤研究(C)
研究期間 : 2011～2013
課題番号 : 23591849
研究分野 : 医歯薬学
科研費の分科・細目 : 内科系臨床医学・放射線科学