瞄准:在 colorectal 癌症上评估 nigericin 的效果并且探索它的可能的机制。方法:人的 colorectal 癌症(CRC ) 房间线 HT29 和 SW480 在指定的条件下面与 nigericin 或 oxaliplatin 被对待。房间生存能力试金和转移试金被执行在 CRC 房间上评估 nigericin 的效果。形成范围的试金和软琼脂形成殖民地的试金被实现在经历的 CRC 房间的癌症干细胞性质上估计 nigericin 的行动上皮间充质的转变(EMT ) 。结果:与 oxaliplatin 相比, nigericin 为 HT29 细胞线显示出更多的毒性(IC50,有 Sw1990 细胞的 12.92 个 ce 异种皮移植模型被造由 lentivirus pGLV3-GFP- miR-95 在 transfection 以后在 vivo 调查胰腺的癌症生长。结果:十 miRNAs 是显著地起来调整的,当时,在 glargine 下面调整的 2 miRNAs 对待 Sw1990 房间与非对待的房间相比(2.48 褶层平均变化, P < 0.01 ) 。miR-95, miR-134 和 miR-34c-3p 是三 miRNAs 由 glargine 调整了的顶(3.65 褶层, 2.67 褶层和 2.60 褶层分别地变化, P < 0.01 ) 在 Sw1990 房间。茎环 RT-PCR 证实了那高剂量 glargine 起来调整在 Sw1990 和 Panc-1 房间的 miR-95 和 miR-134 的表示。最明显的变化是 miR-95 的明显的增加。miR-95 的强迫的表示显著地增加了房间增长(Sw1990:由测量全部的盲肠的 microflora, Bacteroidetes, Firmicutes 和 enterobacteria 的进化的 2.510 olymerase 链反应(qPCR ) 。结果:尽管铁的铁在幼年期重复了管理,在少年时期的既不铁也不铁的铁日报暴露在成人生活在控制动物导致任何效果有限重量获得。铁的铁是不能的限制试验性的大肠炎(1.71 ???? ????? ì
AIM: To evaluate the effect of nigericin on colorectal cancer and to explore its possible mechanism. METHODS: The human colorectal cancer (CRC) cell lines HT29 and SW480 were treated with nigericin or oxaliplatin under the conditions specified. Cell viability assay and invasion and metastasis assay were performed to evaluate the effect of nigericin on CRC cells. Sphereforming assay and soft agar colony-forming assay were implemented to assess the action of nigericin on the cancer stem cell properties of CRC cells undergone epithelial-mesenchymal transition (EMT). RESULTS: Compared with oxaliplatin, nigericin showed more toxicity for the HT29 cell line (IC50, 12.92 ± 0.25 μmol vs 37.68 ± 0.34 μmol). A similar result was also obtained with the SW116 cell line (IC50, 15.86 ± 0.18 μmol vs 41.02 ± 0.23 μmol). A Boyden chamber assay indicated that a significant decrease in the number of HT29 cells migrating through polyvinylidene fluoride membrane was observed in the nigericin-treated group, relative to the vehicle-treated group [11 ± 2 cells per high-power field (HPF) vs 19.33 ± 1.52 cells per HPF, P 〈 0.05]. Compared to the control group, the numbers of HT29 cells invading through the Matrigel-coated membrane also decreased in the nigericin-treated group (6.66 ± 1.52 cells per HPF vs 14.66 ± 1.52 cells per HPF, P 〈 0.05). Nigericin also reduced the proportion of CD133+ cells from 83.57% to 63.93%, relative to the control group (P 〈 0.05). Nigericin decreased the number of spheres relative to the control group (0.14 ± 0.01 vs 0.35 ± 0.01, P 〈 0.05), while oxaliplatin increased the number of spheres relative to the control group (0.75 ± 0.02 vs 0.35 ± 0.01; P 〈 0.05). Nigericin also showed a decreased ability to form colonies under anchorage-independent conditions in a standard soft agar assay after 14 d in culture, relative to the control group (1.66 ± 0.57 vs 7 ± 1.15, P 〈 0.05), whereas the colony numbers were higher in the oxaliplatin gro