突变的细胞只有通过细胞成瘾蜕变为超级竞争者才能发展成为肿瘤。细胞成瘾过程包括早期普通增殖和晚期超级增殖。前期研究表明，促进早期普通增殖可以抑制细胞成瘾。本项目用小鼠结肠癌CT-26细胞作为模型，研究来自发光二极管的640 nm红光（RLED）抑制谷氨酰胺成瘾的应激机制。首先选择无地塞米松休克的普通增殖和有地塞米松休克的细胞成瘾的最佳条件，将细胞成瘾分为早期、中期和晚期；用基因芯片和蛋白质芯片揭示最佳普通增殖和细胞成瘾晚期超级增殖的信号转导通路；然后研究在细胞成瘾各期实施RLED照射对细胞成瘾的抑制作用，并优化RLED照射参数；用荧光定量聚合物链式反应和蛋白质印迹分别研究第三类组蛋白去乙酰化酶、周期蛋白2和普通增殖与细胞成瘾晚期超级增殖信号转导通路的关键蛋白酶的基因表达和蛋白质水平，揭示应激蛋白和信号转导通路在RLED效应中的介导作用，阐明细胞成瘾的抑制机制，为癌症的防治提供理论依据。

The transition of mutated cells from stressed cells to super competitors through cell addiction is the point of tumourigenicity. The process of the cell addition includes early conventional proliferation and late super-competitional proliferation. Our primary studies found that promoting early conventional proliferation may inhibit the cell addiction. The colon carcinoma CT-26 cells were used to study the inhibition of red light at 640 nm from light emitting diode array (RLED) on glutamine addiction and its stressed mechanism. Firstly, the optimum media for conventional proliferation without dexamethasone shock and cell addiction with dexamethasone shock was chosen, the process of the cell addiction was divided into early phase, metaphase and late phase, and the optimum conventional proliferation and the late super-competitional proliferation of the optimum addiction were assessed with gene chips and protein chips, respectively. Secondly, the inhibition of RLED in the early phase, metaphase and late phase of the optimum glutamine addiction and their dosage relationship were studied, and the expression level and protein level of sirtuin 1, period 2, the key kinases of the signal transduction pathways maintaining the conventional proliferation without dexamethasone shock and the late super-competitional proliferation of optimum addiction were studied by real-time fluorescence quantitative polymerase chain reaction and Western Blot, respectively, to find the mediated roles of stress proteins and signal transduction pathways in RLED effects, which will provide the foundation of cancer prevention and treatment.