中文摘要：

黑瘤联系区别的 gene-7 (mda-7 ) ， IL-24，有没有损害正常房间，导致癌症房间 apoptosis 的特定的功能。我们系统地考察 apoptotic 信号小径和他们 Ad.IL-24 和 IL-24 在多样的癌症房间导致的规章的机制。IL-24 能参予改变的信号 transduction 小径，包括 JAK， p38 MAPK， Wnt/-catenin， JNK，嗯应力和联系线粒体的信号小径。并且我们考察与 IL-24 交往的五蛋白质包括 Bip/GRP78， S1R， PKR， Beclin1 和可溶的 clusterin，它相对 IL-24 的肿瘤特定的效果。这被推测嗯应力， G 蛋白质小径和 MAPK 信号小径可以是激活导致 IL-24 在肿瘤房间导致的 apoptosis 的顺序的下游的调停人的主要在上游的受动器。试验性的结果也证明 IL-24 敏化癌症房间并且间接地自己作为直接 apoptosis inducer 支持 apoptosis 而非功能。

英文摘要：

The melanoma differentiation-associated gene-7（mda-7）,IL-24,has the specific functions that induce cancer cell apoptosis without doing harm to normal cells. We systematically review the apoptotic signal pathways and their regulatory mechanisms induced by Ad.IL-24 and IL-24 in diverse cancer cells. IL-24 can participate in varied signal transduction pathways,including JAK,p38 MAPK,Wnt/β-catenin,JNK,ER stress and mitochondria-associated signal pathways. And we review five proteins interacting with IL-24,including Bip/GRP78,S1 R,PKR,Beclin1 and soluble clusterin,which are relative to the tumor-specific effect of IL-24. It is speculated that ER stress,G-protein pathways and MAPK signal pathways may be the primary upstream effectors which activate the sequential downstream mediators resulting in apoptosis induced by IL-24 in tumor cells. Experimental results also show that IL-24 sensitizes cancer cells and indirectly promotes apoptosis rather than functions as a direct apoptosis inducer itself.