Apoptotic Signal Pathways and Regulatory Mechanisms of Cancer Cells Induced by IL-24

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. I...

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Bibliographic Details
Published in:Wuhan University journal of natural sciences 2016-12, Vol.21 (6), p.519-530
Main Authors: Liu, Huilin, Chen, Jiaojiao, Jiang, Xingyan, Wang, Tao, Xie, Xiaoyuan, Hu, Hui, Yu, Fang, Wang, Xingzhi, Fan, Handong
Format: Article
Language:English
Subjects:
Apoptosis
Biomedical and Life Sciences
Cancer
Clusterin
Computer Science
Differentiation
Downstream effects
Effectors
Interleukin 24
JNK protein
Life Sciences
MAP kinase
Materials Science
Mda-7 protein
Melanoma
Mitochondria
Proteins
Regulatory mechanisms (biology)
Review
Signal transduction
Transduction
Tumor cells
Wnt protein
β-Catenin
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Summary: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.
ISSN:1007-1202
1993-4998
DOI:10.1007/s11859-016-1205-2