ArticleCancer research2016
NOTCH Signaling Regulates Asymmetric Cell Fate of Fast- and Slow-Cycling Colon Cancer-Initiating Cells.
Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 64 citations in OpenAlex.
- Targeting asymmetric division in cancer stem cells: implications for relapse and resistance.Cancer cell international · 2025Review
- Dual states of murine Bmi1-expressing intestinal stem cells drive epithelial development utilizing non-canonical Wnt signaling.Developmental cell · 2025Article
- Impact of enzymatic isolation on the propagation efficiency of patient-derived colorectal cancer organoids.Scientific reports · 2025Article
- Canonical and noncanonical NOTCH signaling in the nongenetic resistance of cancer: distinct and concerted control.Frontiers of medicine · 2025Review
- Notch signaling in cancers: mechanism and potential therapy.Frontiers in cell and developmental biology · 2025Review
- Interconnection of CD133 Stem Cell Marker with Autophagy and Apoptosis in Colorectal Cancer.International journal of molecular sciences · 2024Review
- Self-Renewal Inhibition in Breast Cancer Stem Cells: Moonlight Role of PEDF in Breast Cancer.Cancers · 2023Article
- A Short-Term Model of Colitis-Associated Colorectal Cancer That Suggests Initial Tumor Development and the Characteristics of Cancer Stem Cells.International journal of molecular sciences · 2023Article
- A human vascularized microtumor model of patient-derived colorectal cancer recapitulates clinical disease.Translational research : the journal of laboratory and clinical medicine · 2023Article
- Distinct but interchangeable subpopulations of colorectal cancer cells with different growth fates and drug sensitivity.iScience · 2023Article
- Notch receptor/ligand diversity: contribution to colorectal cancer stem cell heterogeneity.Frontiers in cell and developmental biology · 2023Review
- Slow-cycling (dormant) cancer cells in therapy resistance, cancer relapse and metastasis.Seminars in cancer biology · 2022Review
- The JMJD Family Histone Demethylases in Crosstalk Between Inflammation and Cancer.Frontiers in immunology · 2022Review
- Asymmetric Cell Division and Tumor Heterogeneity.Frontiers in cell and developmental biology · 2022Review
- Asymmetric cell division of mammary stem cells.Cell division · 2021Review
- High Expression of Stem Cell-Related Genes in Polyps with Villous Features and High-Grade Dysplasia Support Malignant Phenotype and Colorectal Carcinogenesis.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- Farnesoid X receptor via Notch1 directs asymmetric cell division of Sox9Stem cell research & therapy · 2021Article
- Identification and Characterization of Cancer Cells That Initiate Metastases to the Brain and Other Organs.Molecular cancer research : MCR · 2021Article
- Subversion of Niche-Signalling Pathways in Colorectal Cancer: What Makes and Breaks the Intestinal Stem Cell.Cancers · 2021Review
- Asymmetric cell division promotes therapeutic resistance in glioblastoma stem cells.JCI insight · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.