期刊
JOURNAL OF CELL SCIENCE
卷 129, 期 7, 页码 1287-1292出版社
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/jcs.182873
关键词
GTPase; Oncogene; PI3K; Rac; Raf; Ral
类别
资金
- National Institutes of Health [F32 CA200313, NCI 5-T32CA009156, CA042978, CA179193, CA175747, CA199235]
- Department of Defense [CA140731]
- Pancreatic Cancer Action Network-AACR
- Lustgarten Foundation
RAS proteins (KRAS4A, KRAS4B, NRAS and HRAS) function as GDP-GTP-regulated binary on-off switches, which regulate cytoplasmic signaling networks that control diverse normal cellular processes. Gain-of-function missense mutations in RAS genes are found in similar to 25% of human cancers, prompting interest in identifying anti-RAS therapeutic strategies for cancer treatment. However, despite more than three decades of intense effort, no anti-RAS therapies have reached clinical application. Contributing to this failure has been an underestimation of the complexities of RAS. First, there is now appreciation that the four human RAS proteins are not functionally identical. Second, with > 130 different missense mutations found in cancer, there is an emerging view that there are mutation-specific consequences on RAS structure, biochemistry and biology, and mutation-selective therapeutic strategies are needed. In this Cell Science at a Glance article and accompanying poster, we provide a snapshot of the differences between RAS isoforms and mutations, as well as the current status of anti-RAS drug-discovery efforts.
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