机构地区:[1]Institute of Aging Research,School of Medicine,Hangzhou Normal University [2]The Third Affiliated Hospital,Sun Yat-Sen University [3]Institute of Microbiology,Jiangxi Academy of Sciences
出 处:《Wuhan University Journal of Natural Sciences》2016年第6期519-530,共12页武汉大学学报(自然科学英文版)
基 金:Supported by the National Program on Key Basic Research Project(973 Program)(2012CB518900);the National Natural Science Foundation of China(31160240,31260621);the 12th Five Years Key Programs for Science and Technology Development of China(2012ZX10002006);the Hangzhou Normal University Supporting Project(PE13002004042);the Natural Science Foundation of China of Jiangxi(20114BAB204016)
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.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.
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