Abstract：
: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 interconversion mechanism between slow- and fast-cycling CCIC. Cancer Res; 76(11); 3411-21. ©2016 AACR.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Srinivasan T,Walters J,Bu P,Than EB,Tung KL,Chen KY,Panarelli N,Milsom J,Augenlicht L,Lipkin SM,Shen Xdoi
10.1158/0008-5472.CAN-15-3198subject
Has Abstractpub_date
2016-06-01 00:00:00pages
3411-21issue
11eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-15-3198journal_volume
76pub_type
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