ArticleOncology reports2018
E‑cadherin regulates proliferation of colorectal cancer stem cells through NANOG.
Article in Oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed.
- Pathological and Clinical Significance of Tumor Budding and Its Association with Epithelial-Mesenchymal Transition in Colorectal Carcinoma: A Retrospective Observational Study.Iranian journal of medical sciences · 2025Observational
- Decoding the role of cancer stem cells in digestive tract tumors: Mechanisms and therapeutic implications (Review).International journal of oncology · 2025Review
- CDH1 genetic variants and its aberrant expression are the risk factors for colorectal cancer metastasis.BMC gastroenterology · 2025Article
- Increased amounts of cell-free DNA released from a culture with a high content of cancer stem cells.Frontiers in cell and developmental biology · 2025Article
- Understanding the autophagic functions in cancer stem cell maintenance and therapy resistance.Expert reviews in molecular medicine · 2024Review
- STAU1-mediated CNBP mRNA degradation by LINC00665 alters stem cell characteristics in ovarian cancer.Biology direct · 2024Article
- c-Fos regulated by TMPO/ERK axis promotes 5-FU resistance via inducing NANOG transcription in colon cancer.Cell death & disease · 2024Article
- Differences and Similarities between Colorectal Cancer Cells and Colorectal Cancer Stem Cells: Molecular Insights and Implications.ACS omega · 2023Article
- Tissue-specific cancer stem/progenitor cells: Therapeutic implications.World journal of stem cells · 2023Review
- TRRAP Enhances Cancer Stem Cell Characteristics by Regulating NANOG Protein Stability in Colon Cancer Cells.International journal of molecular sciences · 2023Article
- NanoacetylatedACS medicinal chemistry letters · 2022Article
- Aspirin sensitivity of PIK3CA-mutated Colorectal Cancer: potential mechanisms revisited.Cellular and molecular life sciences : CMLS · 2022Review
- Article
- Stemness, Inflammation and Epithelial-Mesenchymal Transition in Colorectal Carcinoma: The Intricate Network.International journal of molecular sciences · 2021Review
- Cancer stem cell characteristics and their potential as therapeutic targets.Medical oncology (Northwood, London, England) · 2021Review
- Biejiajian Pill Inhibits Carcinogenesis and Metastasis via the Akt/GSK-3β/Snail Signaling Pathway in Hepatocellular Carcinoma.Frontiers in pharmacology · 2021Article
- The Association Between Inflammation, Epithelial Mesenchymal Transition and Stemness in Colorectal Carcinoma.Journal of inflammation research · 2020Article
- miR-219 regulates liver cancer stem cell expansion via E-cadherin pathway.Cell cycle (Georgetown, Tex.) · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer stem cells (CSCs) possess a self‑renewal ability and display tumorigenic potential in immunodeficient mice. Colorectal CSCs are thought to be a uniform population and no functionally distinct subpopulations have been identified. Because E‑cadherin is an essential molecule for self‑renewal of embryonic stem cells, we examined E‑cadherin expression, which may play a role in maintaining the properties of CSCs, in EpCAMhigh/CD44+ colorectal CSCs from human primary colorectal cancers. We obtained 18 surgical specimens of human primary colorectal cancer. CD44, EpCAM, and E‑cadherin expression were analyzed by fluorescence‑activated cell sorting. Sorted EpCAMhigh/CD44+ colorectal CSCs were injected into immunodeficient mice to estimate the tumorigenic potential. Genetic profiles were analyzed by cDNA microarray. Notably, colorectal CSCs could be divided into two populations based on the E‑cadherin expression status, and they exhibited different pathological characteristics. Compared to E‑cadherin‑negative colorectal CSCs, E‑cadherin‑positive (EC+) colorectal CSCs demonstrated higher tumor growth potential in vivo. EC+ colorectal CSCs revealed a higher expression of the pluripotency factor NANOG, which contributed to the higher tumor growth potential of EC+ colorectal CSCs through control of cyclin D1 expression. These findings are the first demonstration of functionally distinct subpopulations of colorectal CSCs in human clinical samples.
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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.