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首页> 外文期刊>Cell cycle >YAP oncogene overexpression supercharges colon cancer proliferation
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YAP oncogene overexpression supercharges colon cancer proliferation

机译：YAP癌基因过表达增强结肠癌的增殖

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摘要

The transcriptional co-activator YAP is an evolutionarily conserved regulator of organ size and progenitor cell proliferation. YAP is overexpressed at high frequency in many common human cancers and can directly drive cancer development in mouse models. YAP abundance and nuclear localization are negatively regulated by the Hippo kinase cascade, which, in epithelia, is activated by physiological cell-cell contact. Recent work in intestinal epithelium has established that YAP is constitutively inhibited by the Hippo pathway and entirely dispensable for normal development and homeostasis. YAP serves only in a standby capacity; should cell-cell contact be abrogated, as after intestinal damage, the loss of Hippo input permits increased YAP abundance and nuclear residence. In turn, YAP cooperates with β-catenin to transactivate genes that promote stem cell expansion for epithelial repair. This interplay between overexpressed YAP and β-catenin also drives proliferation of colon cancer cells. The dispensability of YAP in normal intestine makes YAP's expression or outputs attractive targets for cancer therapy.
机译：转录共激活因子YAP是器官大小和祖细胞增殖的进化保守调节子。 YAP在许多常见的人类癌症中高表达，可以直接驱动小鼠模型中的癌症发展。 YAP丰度和核定位受Hippo激酶级联反应的负调控，而Hippo激酶级联反应在上皮细胞中通过生理性细胞间接触而激活。肠上皮的最新研究表明，YAP被Hippo途径组成型抑制，对于正常发育和体内平衡完全不可。 YAP仅在备用状态下服务;如果废除细胞与细胞的接触，如肠损伤后，河马输入的损失会增加YAP的丰度和核的滞留。反过来，YAP与β-catenin协同激活激活干细胞扩增的基因以上皮修复。过表达的YAP和β-连环蛋白之间的这种相互作用也驱动结肠癌细胞的增殖。 YAP在正常肠中的可分配性使YAP可以表达或输出有吸引力的癌症治疗靶标。

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