Myc inhibits JNK-mediated cell death in vivo
Myc inhibits JNK-mediated cell death in vivo
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Myc 抑制体内 JNK 介导的细胞死亡
DOI：
10.1007/s10495-016-1340-4
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发表时间：
2017-04-01
期刊：
影响因子：
7.2
通讯作者：
Xue, Lei
中科院分区：
文献类型：
--
作者：
Huang, Jiuhong;Feng, Yu;Xue, Lei
原癌基因Myc以其在促进细胞生长、增殖和凋亡中的作用而广为人知。然而，在本研究中，我们通过基因筛选发现，在果蝇中Myc抑制而非促进由c-Jun氨基末端激酶（JNK）信号传导引发的细胞死亡。首先，果蝇Myc（dMyc）的表达会抑制异位激活的JNK信号诱导的细胞死亡，而dMyc缺失则会增强这种细胞死亡。其次，dMyc会阻碍生理激活的JNK通路介导的细胞死亡。第三，dMyc缺失会触发JNK通路激活以及JNK依赖性细胞死亡。最后，哺乳动物cMyc基因在果蝇中表达时，会阻碍激活的JNK信号诱导的细胞死亡。因此，除了其已被充分研究的促进凋亡功能外，Myc在果蝇中还拮抗JNK介导的细胞死亡，并且这种功能很可能从果蝇到人类都是保守的。
The proto-oncogene Myc is well known for its roles in promoting cell growth, proliferation and apoptosis. However, in this study, we found from a genetic screen that Myc inhibits, rather than promotes, cell death triggered by c-Jun N-terminal kinase (JNK) signaling inDrosophila. Firstly, expression ofDrosophilaMyc (dMyc) suppresses, whereas loss ofdMycenhances, ectopically activated JNK signaling-induced cell death. Secondly, dMyc impedes physiologically activated JNK pathway-mediated cell death. Thirdly, loss of dMyc triggers JNK pathway activation and JNK-dependent cell death. Finally, the mammaliancMycgene, when expressed inDrosophila, impedes activated JNK signaling-induced cell death. Thus, besides its well-studied apoptosis promoting function, Myc also antagonizes JNK-mediated cell death inDrosophila, and this function is likely conserved from fly to human.