Objective:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) holds promise for cancer therapy as it has unique capacity to selectively trigger apoptosis in cancer cells. We reported here that paclitaxel sensitized gastric cancer cells to TRAIL-induced apoptosis.Methods: After drug exposure, apoptosis rate and caspase activation were examined. Various proteins were detected by western blot. Several interventions, including pharmacological inhibitors and siRNA transfection were used. hTe growth inhibition of tumors was evaluated in SGC-7901-implanted nude mice model.Results:We found gastric cancer cellsshowed a mixed response to TRAIL. Combined treatment with paclitaxel markedly enhanced TARIL-induced apoptosis in vitro and in vivo. The underlying mechanisms involved in synergistical activation of caspase proteins, up-regulation of receptors, down-regulation of antiapoptotic proteins and inactivation of MAPKs.Conclusion:TRAIL-induced cytotoxicity and apoptosis can be synergistically enhanced by paclitaxel, suggesting the therapeutic potential of combining TARIL plus paclitaxel in gastric cancer treatment.

TAT-tCNTF对CD诱导HUVEC细胞损伤的作用研究

目的探讨TAT-tCNTF对细胞松弛素D（CD）诱导人脐静脉内皮细胞（HUVEC）损伤作用的影响。方法 CCK-8法检测TAT-tCNTF对CD致HUVEC生长抑制的作用；荧光显微镜检测CD诱导HUVEC的F-actin的变化，以及在TAT-tCNTF作用下对细胞微丝的影响；荧光显微镜和流式细胞术检测CD和TAT-tCNTF作用后细胞内Ca2+浓度；Western blot检测CD和TAT-tCNTF作用后F-actin的蛋白水平的变化。结果在1μg·ml-1的CD作用HUVEC后，细胞表现出明显的生长抑制，而在0.05~10μg·ml-1浓度范围内，TAT-tCNTF促进HUVEC的生长，并可改善CD对HUVEC的损伤，TAT-tCNTF组与CD+TAT-tCNTF组细胞活动度具有明显差异；荧光显微镜下检测到经CD作用后细胞F-actin分布减少，而经TAT-tCNTF作用后细胞F-actin分布密集；采用Fluo 4-AM荧光探针标记细胞内Ca2+浓度，荧光显微镜和流式细胞术检测到TAT-tCNTF能够降低经CD损伤HUVEC后的细胞内Ca2+浓度升高；FCM检测显示，CD组的MFI相对于对照组明显增加，而CD+TAT-tCNTF组MFI较CD组明显降低。Western blot显示各组之间的F-actin表达量没有明显改变。结论TAT-tCNTF对CD致内皮细胞的损伤有改善和逆转作用，其改善机制可能与增加细胞活性和维持细胞骨架有关。