No back seat for a progression event-K-RAS as a therapeutic target in CRC.
No back seat for a progression event-K-RAS as a therapeutic target in CRC.
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DOI：
10.1101/gad.297630.117
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发表时间：
2017-02-15
影响因子：
10.5
通讯作者：
Haigis KM
中科院分区：
文献类型：
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作者：
Poulin EJ;Haigis KM
在这篇展望中，Poulin和Haigis讨论了Boutin等人的一项研究，该研究提出了一种新的CRC小鼠模型，其中致癌K-RAS的表达受强力霉素调节。KRAS是人类癌症中最常见的突变癌基因，在结直肠癌（CRC）进展中起着重要作用，尽管人们对此知之甚少。在这期《基因与发育》杂志上，Boutin及其同事（第100页）370-382）提出了一种新的CRC小鼠模型，其中致癌K-RAS的表达受多西环素调节。使用该模型，他们证明了致癌K-RAS的持续表达是原发性和转移性结肠癌生存所必需的，并且致癌K-RAS激活TGF-β信号传导以促进肿瘤侵袭和转移。
In this Outlook, Poulin and Haigis discuss a study from Boutin et al. that presents a new mouse model of CRC in which the expression of oncogenic K-RAS is regulated by doxycycline. KRAS is the most frequently mutated oncogene in human cancer and plays a central, although poorly understood, role in colorectal cancer (CRC) progression. In this issue of Genes & Development, Boutin and colleagues (pp. 370–382) present a new mouse model of CRC in which the expression of oncogenic K-RAS is regulated by doxycycline. Using this model, they demonstrate that continued expression of oncogenic K-RAS is required for the survival of primary and metastatic colon cancers and that oncogenic K-RAS activates TGF-β signaling to promote tumor invasion and metastasis.