Journal
CANCER RESEARCH
Volume 76, Issue 11, Pages 3411-3421Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-15-3198
Keywords
-
Categories
Funding
- NCATS NIH HHS [UL1 TR001414] Funding Source: Medline
- NIGMS NIH HHS [R01 GM114254, R01 GM095990] Funding Source: Medline
- Div Of Chem, Bioeng, Env, & Transp Sys
- Directorate For Engineering [1350659] Funding Source: National Science Foundation
Ask authors/readers for more resources
Colorectal cancer cells with stem-like properties, referred to as colon cancer-initiating cells (CCIC), have high tumorigenic potential. While CCIC can differentiate to promote cellular heterogeneity, it remains unclear whether CCIC within a tumor contain distinct subpopulations. Here, we describe the co-existence of fast-and slow-cycling CCIC, which can undergo asymmetric division to generate each other, highlighting CCIC plasticity and interconvertibility. Fast-cycling CCIC express markers, such as LGR5 and CD133, rely on MYC for their proliferation, whereas slow-cycling CCIC express markers, such as BMI1 and hTERT, are independent of MYC. NOTCH signaling promotes asymmetric cell fate, regulating the balance between these two populations. Overall, our results illuminate the basis for CCIC heterogeneity and plasticity by defining a direct inter-conversion mechanism between slow-and fast-cycling CCIC. (C) 2016 AACR.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available