期刊
CANCER CELL
卷 21, 期 6, 页码 777-792出版社
CELL PRESS
DOI: 10.1016/j.ccr.2012.04.036
关键词
-
资金
- Princess Margaret Hospital
- Genome Canada through the Ontario Genomics Institute
- Ontario Institute for Cancer Research
- province of Ontario
- Canadian Institutes for Health Research
- Canada Research Chair
- Ontario Ministry of Health and Long Term Care (OMOHLTC)
There is increasing evidence that some cancers are hierarchically organized, sustained by a relatively rare population of cancer-initiating cells (C-ICs). Although the capacity to initiate tumors upon serial transplantation is a hallmark of all C-ICs, little is known about the genes that control this process. Here, we establish that ID1 and ID3 function together to govern colon cancer-initiating cell (CC-IC) self-renewal through cell-cycle restriction driven by the cell-cycle inhibitor p21. Regulation of p21 by ID1 and ID3 is a central mechanism preventing the accumulation of excess DNA damage and subsequent functional exhaustion of CC-ICs. Additionally, silencing of ID1 and ID3 increases sensitivity of CC-ICs to the chemotherapeutic agent oxaliplatin, linking tumor initiation function with chemotherapy resistance.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据